International Journal of Myeloma 2019, 9（1）International Journal of Myeloma 2019,（9 ）1 

日本骨髄腫学会誌

International Journal of Myeloma

個性に基づく骨髄腫治療時代の幕開け

プログラム・抄録集

第四十四回
日本骨髄腫学会学術集会
プログラム・抄録集

会期

会場
会長

第44回 日本骨髄腫学会学術集会
プログラム・抄録集

目次

会長挨拶‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥ 3
プログラム編成と一般演題（プレナリー・ポスター）の‥査読・評価の方法について‥ ‥‥‥‥‥‥‥‥‥‥‥‥‥ 4
アクセスマップ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥ 5
会場案内図‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥ 6
参加者へのご案内‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥ 7
発表者へのご案内‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥ 9
ポスター発表のご案内‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥12
座長へのご案内‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥13
会議・懇親会のご案内‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥13
日程表（Schedule）‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥14
プログラム（Program）‥ ‥‥‥‥‥‥‥‥‥‥‥‥‥‥19
会長講演（Presidential Lecture）‥‥‥‥‥‥‥‥‥‥‥49
シンポジウム（Symposium）‥‥‥‥‥‥‥‥‥‥‥‥‥53
Pros and Cons‥ ‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥65
プレナリー（Plenary）‥ ‥‥‥‥‥‥‥‥‥‥‥‥‥‥69
ポスター発表（Poster Presentation）‥‥‥‥‥‥‥‥‥81
共催セミナー（Co-sponsored Seminars）‥‥‥‥‥‥ 177
次回学術集会のご案内‥‥‥‥‥‥‥‥‥‥‥‥‥‥ 189
過去の学術集会一覧‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥ 190
協賛企業一覧‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥‥ 191

第 44 回日本骨髄腫学会学術集会 事務局
名古屋市立大学大学院医学研究科 血液・腫瘍内科学〒 467-8601 愛知県名古屋市瑞穂区瑞穂町字川澄 1

会長挨拶

第 44 回日本骨髄腫学会学術集会（名古屋市立大学大学院医学研究科

飯田会長
血液・腫瘍内科学）真介

第 44 回日本骨髄腫学会学術総会を 2019 年 5 月 11 日、12 日の 2 日間、名古屋駅近くのウ
インクあいちにて開催させていただきます。愛知県での開催は、2004 年に清水一之先生が名古屋市で開催されてから 15 年ぶりとなります。ボルテゾミブの我が国での承認が 2006 年ですから、当時は新規薬剤のない時代でした。現在は、プロテアソーム阻害薬、免疫調節薬、ヒスト
ン脱アセチル化酵素阻害薬、抗体薬といった多様な薬剤選択が可能となり、さらなる新規薬剤
や細胞免疫療法の開発も続いています。治療選択肢は増え骨髄腫患者さんの予後は年々改善しつつありますが、未治療多発性骨髄腫は主に移植適応か非適応かという視点から標準治療が決められています。再発・難治性骨髄腫についても、患者さん毎に疾患の病態や臓器機能、合併症に応じて適切な治療が選択されていますでしょうか。平成から新たな時代への移行期に、我が国にもゲノム医療時代が訪れようとしています。本学会が、骨髄腫の分子病型に応じた治療選択、合併症に応じた治療選択、高齢者の包括的機能評価を考慮した治療選択、微小残存腫瘍（MRD）陰性化を目指す治療選択 vs CRAB 症候のない長期病状安定を目指す治療選択といった患者さん毎に最適な治療「個性に基づく骨髄腫治療」を考える機会になれば幸いです。
本学会のテーマである「個性に基づく骨髄腫治療時代の幕開け」に相応しい３つのシンポジ
ウム「染色体と分子病態に基づくリスクに応じた骨髄腫治療の層別化」、「合併症の病態に基づく骨髄腫の最適な治療選択」、「骨髄腫領域の診断および治療における技術革新」と、２つのス
ポンサードシンポジウム「高齢者骨髄腫の治療」、「多発性骨髄腫治療における MRD の意義」、
さらに Pros & Cons「自家移植後の維持療法は必要か？どのような患者が適応で、どのような維持療法が良いのか？」を企画しました。一般演題はプレナリーとポスターセッションに分けています。プレナリーセッションはプログラム委員の査読に基づいて領域毎に優れた演題を選出しておりますが、ポスター演題も優秀演題を含め興味深い演題が満載です。本学会はポスター
会場での活発な議論と交流を重視したプログラム構成にしており、ポスターは 2 日間通して掲
示いただけるように配慮致しました。
名古屋駅周辺は近年目覚ましい開発が進んでいます。会員懇親会は、名古屋飯を堪能いただ
きながら楽しい交流の場にしていただけるよう工夫しておりますので、奮ってご参加ください。
最後に、本学術集会の開催に絶大なご協力をいただきましたプログラム・査読委員の先生、学会事務局の皆様に厚く御礼申し上げます。
3

プログラム編成と一般演題（プレナリー・ポスター）の査読・評価の方法について
本学術集会のプログラム編成および一般演題の査読・評価方法について、以下のように進めましたので、会員の皆様にご報告いたします。

1）プログラム委員は、日本骨髄腫学会の代議員 21 名で構成されました。

2）‌以下の 4 項目でプログラム委員に採点をしていただき、その採点結果に基づき会長・事務局長・
プログラム委員長がプログラム案を作成いたしました。

①倫理構成 / 記述の正確性②方法・結果の妥当性③重要性 / 貢献度

3）一般演題は、以下の 8 つのカテゴリで募集をさせていただきました。

④新規性 / オリジナリティ①病因・病態に関する基礎研究②治療に関する基礎研究⑥治療（再発）に関するもの⑦合併症・支持療法・コメディカルに関するもの④治療（移植）に関する臨床研究③症例報告⑤治療（非移植）に関する臨床研究⑧アミロイドーシス・POEMS に関するもの

その結果、国内外で計 104 演題のご応募をいただきました。

4）‌一般演題の査読は、プログラム委員 21 名によって行われました。各演題につき 2 名が独立して査読を行い、判定基準に従って 1 ～ 5 点の 5 段階で評価しました。

5）‌査読の評価とカテゴリも考慮した会長の審査により一般演題の中からプレナリー、優秀ポスターを選定しました。

受賞者の皆様におかれましては、‌受賞者の表彰は 5 月 11 日（土）の懇親会にて行われます。なお、懇親会にご招待いたしますので、参加受付にてお申し出下さいますよう御願いいたします。

ご協力いただきましたプログラム委員を掲載させていただき、この場を借りて深謝いたします。
第 44 回日本骨髄腫学会学術集会

プログラム委員麻奥英毅（広島赤十字・原爆病院

石田禎夫（日本赤十字社医療センター

安倍
伊藤
今井
尾崎
黒田
小杉
柴山
角南
高松
田村
張

正博（徳島大学大学院検査部）

薫樹（岩手医科大学

医歯薬学研究部

修治（徳島県立中央病院
純也（京都府立医科大学

血液・腫瘍内科）

血液内科）

浩彦（大阪大学大学院

医学系研究科秀人（日本医科大学附属病院

4

血液・呼吸器内科）

血液内科）

高明（新潟県立がんセンター新潟病院
豊（慶應義塾大学薬学部

内科）

血液内科）

病理生理学講座）尚也（千葉大学医学部附属病院

李

血液内科）

博幸（金沢大学大学院医学系研究科

三村安井

血液・腫瘍内科）

一貴（国立病院機構岡山医療センター一朗（愛知医科大学病院

村上

血液腫瘍内科）

血液内科）

花村
半田

血液内科）

臨床腫瘍学講座）

中世古知昭（国際医療福祉大学医学部
服部

血液・内分泌代謝内科学）

陽一（東京大学医科学研究所附属病院

浩史（大垣市民病院※敬称略、50 音順

血液内科）

寛（群馬大学医学部附属病院

血液内科）

輸血・細胞療法部）

博和（群馬大学大学院保健学研究科

寛（東京大学医科学研究所附属病院

保健学専攻

生体情報検査科学講座）

政樹（名古屋市立大学大学院医学研究科

血液腫瘍内科）

血液・腫瘍内科学）アクセスマップ

JR
名古屋駅

JR
セントラル
タワーズ

堀内ビル

泥江町

近鉄名古屋線
名鉄名古屋本線

あおなみ線

地下鉄桜通線

桜通
名古屋
ユニモール地下街
ビルディング 5 番出口

キャッスル
プラザ

名古屋
第二埼玉ビルウインクあいち

柳橋中央市場

名鉄
名古屋駅
近鉄
名古屋駅

名古屋
国際
センター

ミッドランドスクエア

名古屋三井ビルディング

センチュリー
豊田ビル

錦通
モード学園

名駅入口

国際センター駅

名古屋高速都心環状線

JR
セントラル
タワーズ

大名古屋
ビルヂング

桜通口

大閣通口

Ｎ

錦橋出口

地下鉄東山線

錦橋東

広小路通
笹島

愛知県産業労働センター 〒450-0002 名古屋市中村区名駅4-4-38（ウインクあいち）

TEL:052-571-6131㈹愛知県産業労働センター（ウインクあいち）へのアクセス

電車をご利用の場合■JR名古屋駅桜通口から…ミッドランドスクエア方面 徒歩5分
各線地下鉄名古屋駅から…ユニモール地下街5番出口 徒歩2分
※各駅地下街サンロードからミッドランドスクエア、マルケイ観光ビル
名古屋クロスコートタワーを経由 徒歩8分
■JR（東海道新幹線）をご利用の場合◎東京…約100分 ◎新大阪…約50分

お車をご利用の場合名古屋高速都心環状線「錦橋」出口より約6分
駐車場…収容台数123台

飛行機をご利用の場合■中部国際空港（セントレア）から…約30分（名鉄空港特急利用、名鉄名古屋駅まで）■県営名古屋空港から…約20分（高速バス利用、ミッドランドスクエア前バス停 まで）

5

会場案内図ウインクあいち2F

参加受付・抄録集販売デスク・ランチョンセミナー整理券配布

運営事務局

第1会場
大ホール

企業展示

エレベーター
B１F～８Fに停止

エレベーター
全フロアに停止

PC受付

8F
クローク
展示・
ホスピタリティスペース

ポスター会場

9階へ
エレベーター
B1F・１・８F 以上に停止

9F
休憩スペース
901

第2会場
902

※ 9 階へは直通エレベーター（1 台のみ）をご利用いただくか、8 階で高層階用エレベーターへお乗り換えください。
また、階段もご利用いただけます。
6

参加者へのご案内

Ⅰ．参加受付
場所：ウインクあいち 2 階

ホワイエ

時間：5 月 11 日（土）8：00 ～ 18：15
5 月 12 日（日）7：30 ～ 15：00

参加費をお支払いのうえ、参加証（領収書兼）を受け取り、氏名・所属をご記入して着用ください。
※参加証を着用されていない方への講演会場等への入場はできません。
参加費（2 日間有効）
医師10,000 円

企業

10,000 円

コメディカル5,000 円患者

新研修制度における初期研修医

2,000 円

無料＊ 1

非 M.D. の大学院生・学部生・留学生＊1＊2「参加費免除申請書」を提示してください。

無料＊ 2「参加費免除申請書」とともに「学生証」を提示してください。

参加費免除申請書はホームページからダウンロード可能です。
抄録集販売

抄録集販売デスクにて 1 冊 1,000 円にて抄録集を販売いたします。

懇親会

場所：名古屋マリオットアソシアホテル 16 階
時間：5 月 11 日（土）19：15 ～
会費：2,000 円
定員：150 名

アイリス

学会参加受付にてお申込みください。
定員に達した段階で締め切ります。

ネームカードを着用してご参加ください。

懇親会にて、プレナリー、優秀ポスターの授賞式を行います。

なお、受賞者の皆様におかれましては、懇親会にご招待いたしますので、総合案内にてお申し出ください。
ランチョンセミナー整理券

ランチョンセミナー時の混雑緩和のため、以下の場所・時間帯に整理券を配布します。
場所：5 月 11 日（土）ウインクあいち 2 階

ホワイエ

参加受付

5 月 12 日（日）ウインクあいち 2 階

ホワイエ

ランチョンセミナー整理券配布デスク

参加受付の際に 5 月 11 日開催のランチョンセミナーのご希望をお伺いいたします。

時間：5 月 11 日（土）8：00 ～ 11：00
5 月 12 日（日）7：30 ～ 11：00

整理券配布の終了時間以降、整理券が残っている場合は、各会場前にて配布いたします。

整理券をお持ちの方からご入場いただきますが、整理券はセミナー開始 5 分後に無効となります。
モーニングセミナー・スポンサードシンポジウム

整理券の配布はございませんので、直接、該当会場にお越しください。

7

参加者へのご案内

Ⅱ．事務局受付
場所：ウインクあいち 2 階

ホワイエ

時間：5 月 11 日（土）10：00 ～ 12：30 ／ 14：00 ～ 17：00
5 月 12 日（日）10：00 ～ 16：00

本年度会費未納の方は「事務局受付」にてお支払いください。
新入会員の入会も受け付けます。
学会年会費
代議員

5,000 円／一般会費

3,000 円

Ⅲ．クローク
場所：ウインクあいち 8 階

801

時間：5 月 11 日（土）8：00 ～ 18：45
5 月 12 日（日）7：30 ～ 17：30※貴重品、パソコン、傘はお預かりできませんので、予めご了承ください。

Ⅳ．休憩スペース
場所：ウインクあいち 8 階
9階

ポスター会場901

時間：5 月 11 日（土）8：00 ～ 18：15
5 月 12 日（日）7：30 ～ 15：00

会期中、上記に休憩スペースを設けております。

電源もございますので、ご自由にご利用ください。

Ⅴ．ホスピタリティスペース・企業展示（8階）
場所：ウインクあいち 8 階

ポスター会場

時間：5 月 11 日（土）10：00 ～ 18：40

5 月 12 日（日） 8：00 ～ 16：00

共催：ヤンセンファーマ株式会社

Ⅵ．企業展示（2階）
場所：ウインクあいち 2 階

ホワイエ

時間：5 月 11 日（土）9：00 ～ 17：00
5 月 12 日（日）8：00 ～ 14：00

Ⅶ．Free Wi-Fiのご案内について
場所：ウインクあいち 8 階
SSID

9階

ポスター会場

第 2 会場（902）、休憩スペース（901）

８階：44jsm01

９階：44jsm02 / 44jsm03 / 44jsm04

PW

８階・９階共通：nagoya20198

発表者へのご案内

Ⅰ．発表形式について
本学術集会では、発表形式を以下の通りとします。

【シンポジウム・Pros and Cons・プレナリー】
スライド：英語のみ

発表言語：日本語、英語どちらでも可

スライドは全て英語でご作成いただきますようお願いいたします。

【ポスター】

ポスター：日本語、英語どちらでも可
発表言語：日本語、英語どちらでも可

Ⅱ．発表データ受付
ご発表の 30 分前までにウインクあいち 2 階の PC 受付にお越しいただき、データの確認、試写を行ってくだ
さい。

受付時間：

5 月 11 日（土）8：00 ～ 18：00
5 月 12 日（日）7：30 ～ 15：30【発表機材】
Windows

Macintosh

PC 本体の持込〇〇

メディアの持込（USB メモリー・CD-R）〇

×

PowerPoint 2010，2013，2016

PowerPoint、Keynote

Windows Media Player―

アプリケーション
動画ソフト※ Macintosh でプレゼンテーションデータを作成された場合はご自身のパソコンをご持参ください。
※本学会は、PC プレゼンテーションのみの発表といたします。

※動画ファイルがある場合は、パソコン本体のお持込みをお奨めいたします。
【データのみ持ち込まれる方へ】

１．当日は発表予定時間の 30 分前までに「PC 受付」
にて試写用パソコンで発表データの確認を行ってください。
（データのお持込みは、発表日以外でも受付けます。）

２．お持込みいただけるメディアは以下の通りです。
・USB フラッシュメモリー
・CD-R※ ‌CD-R の書き込みはハイブリッドフォーマットをお使いください。パケットライトなど特殊な機能は読み込み時の不具合の原因になりますのでご使用にならないでください。

※‌メディアは、ウイルス定義データを最新のものに更新された状態のセキュリティーソフトで、メディアにウイルスが感染していないことをご確認いただいた上でお持込みください。

３．OS とアプリケーションは以下のものをご用意します。
・OS：Windows・アプリケーション：Windows 版 PowerPoint 2010、2013、2016

４．フォントは OS（Windows）に標準のもののみ、ご用意いたします。

５．‌発表に使用する PC は全て XGA（1024 × 768）に統一してありますので、ご使用の PC の解像度を XGAに合わせてからレイアウトをご確認ください。

9発表者へのご案内

６．動画や音声をご使用になる場合は、データ登録の際に必ずお知らせください。

７．‌ファイル名は「演題番号 _ 演者名 .ppt」もしくは「演題番号 _ 演者名 .pptx」としてください。
（例：O-1_
骨髄腫太郎 .ppt）※「.ppt」、「.pptx」は拡張子（英数半角）です。

８．動画などの参照ファイルがある場合は、全てのデータを同じフォルダに入れてください。
※動画ファイルの注意点‌Windows の場合 Windows10（OS）及び WindowsMediaPlayer12 の初期状態に含まれるコーデックで再生できる動画ファイルをお持ちください。（動画ファイルは WMV 形式を推奨します。）

９．発表データ作成後、作成したパソコン以外のパソコンで正常に動作するかチェックしてください。
10．発表会場ではデータの修正はできませんので、予めご了承ください。
11．試写が終了しましたらデータはご発表会場まで転送されます。

12．‌発表時には、ご発表データの 1 枚目をスライドショー状態でスクリーンに映写しますので、演台上のマウ
ス、キーパッドで、ご自身でデータの送りの操作を行ってください。

「PC 受付」のサーバと会場のパソコンにご発表データを一時保存いたしますが、これら
13．‌ご発表データは、のデータは本学会終了後、責任を持って廃棄します。

【ノートパソコンを持ち込まれる方へ】

１．発表予定時間の 30 分前までに「PC 受付」へお越しください。

２．
「PC 受付」の試写用モニターにてケーブルの接続を確認してください。

３．
「PC 受付」では D-Sub15 ピン（ミニ）のケーブルをご用意いたします。

４．‌一部のノートパソコンでは本体附属（別売り）のコネクターが必要な場合がありますので、必ずお持ちください。

D-sub15 ピン（ミニ）付属外部出力ケーブル

例５．ノートパソコンから外部モニターに正しく出力されるか確認してください。

６．個々のパソコンや OS により設定方法が異なりますので、事前にご確認ください。

７．‌デスクトップ上の分かりやすい場所に発表データのショートカット（エイリアスを「演題番号 _ 演者名」
として作成してください。
（例：O-1_ 骨髄腫太郎）

８．画面の解像度は XGA（1024 × 768）です。

９．動画や音声をご使用になる場合は、発表データ確認の際に必ずお知らせください。
10．予め、スクリーンセーバー、省電力設定を解除してください。

11．起動時にパスワード等を設定している場合は、必ず解除しておいてください。

12．‌会場にて電源をご用意しておりますので、AC アダプターを必ずお持ちください。ご発表予定時間の 30

分前位（講演中でもかまいません）に会場内左手前方演台付近の PC デスクまでお越しのうえ、スタッフに、PC をお渡しください。スタッフが、ケーブルを接続し、外部出力の確認を行います。

13．‌ご発表時には、演台にセットされているモニター、マウス、キーパッドをご使用ください。発表者ツールのご使用はできません。

14．念のため、バックアップデータを必ずお持ちください。

15．発表会場ではデータの修正はできませんので、予めご了承ください。

16．‌先に PC を預けた会場内左手前方演台付近の PC デスクで、パソコンをご返却いたします。講演終了後 PC
デスクのスペースの問題がありますので、出来るだけ速やかに PC のお引取りをお願いします。

10

発表者へのご案内

Ⅲ．発表について
ご自身の発表の 10 分前にはスクリーンに向かって左前方の次演者席にお越しください。

発表時間は以下の通りです。セッションの進行は、座長の指示に従い、時間厳守でお願いします。
セッション

発表時間

シンポジウム

討論・質疑時間

セッションごとに設定

Pros and Cons

25 分

20 分（討論）

プレナリー

9分

3 分（質疑）Ⅳ．利益相反の開示について発表スライドの最初または、演題・発表者などを紹介するスライドの次に利益相反（COI）状態を開示してください。

COI スライドはホームページからダウンロード可能です。

11

ポスター発表のご案内

Ⅰ．発表・貼付・撤去時間
貼付

5 月 11 日（土）8：30 ～ 10：00

5 月 12 日（日）8：00 ～ 15：50

閲覧

5 月 11 日（土） 10：00 ～ 18：30

発表

5 月 11 日（土） 17：10 ～ 18：30

撤去

5 月 12 日（日） 16：00 ～ 17：00

5 月 12 日（日） 14：30 ～ 15：50

Ⅱ．ポスター作成方法
・ポスター掲示面の大きさは幅 90cm、高さ 210cm です（サンプル参照）。
（演題番号は、学会事務局
・‌パネルの左肩に演題番号が表示されます。

【掲示ポスターサンプル】

にて用意します）・‌発表者は、指定のパネル上部の演題番号を除くスペースに演題名、所属、演者、氏名とすべての共同演者氏名を提示してください。

20cm

70cm

20cm

演題 演題タイトル・所属・氏名
番号

170cm

貼付スペース

・本文はその下のスペースに掲示してください。
・画鋲はポスター会場に用意します。

・ポスターの言語は日本語、英語どちらでも構いません。
・利益相反についても明示ください（前項参照）。

Ⅲ．発表について・‌ポスター発表開始の 5 分前には自身のポスターの前にお越しください。

・発表時間 4 分、討論時間 2 分です。

・セッションの進行は、座長の指示に従い、時間厳守でお願いします。
・発表言語は日本語、英語どちらでも構いません。

Ⅳ．注意事項・‌ポスター発表は 2 日間に分けて行いますが、ポスター貼付は 1 日目

から可能で、
ポスター撤去は 2 日目の夕方（5 月 12 日 16 時～ 17 時）

20cm

20cm

利益相反
（COI）

30cm

に行って下さい。参加者がポスター閲覧可能な時間をできる限り長くする目的で、ポスターの掲示は原則 2 日間お願いいたします。

・‌撤去時間を過ぎてもお引き取りのないポスターは、学会事務局で撤去し、プログラム終了時に廃棄いたしま
すのでご了承ください。

12

座長へのご案内、会議・懇親会のご案内

Ⅰ．口演
座長をされるセッションの 10 分前には、スクリーンに向かって右前方の次座長席にお越しください。

Ⅱ．ポスター
会場前の座長受付にお立ち寄りください。
指示棒をお渡しいたします。

会議・懇親会のご案内
理事会

2019 年 5 月 10 日（金）14：30 ～ 15：30
ウインクあいち 9 階

904

代議員会

2019 年 5 月 10 日（金）15：45 ～ 16：45
ウインクあいち 9 階

903

懇親会

2019 年 5 月 11 日（土）19：00 ～ 21：15
名古屋マリオットアソシアホテル
懇親会費：2,000 円
定員：150 名

16 階

アイリス

定員に達した段階で締め切ります。

参加ご希望の方は学会参加受付にてお申込みください。
ネームカードを着用してご参加ください。

13

日程表
5 月 11 日（土）
会場名

第1会場

第2会場

ポスター会場

部屋名

大ホール
（2F）

902
（9F）

展示場
（8F）

8:00

9:00

10:00

11:00

8：50－9：00

開会式
掲示
8：30－10：00

シンポジウム1
9：00－10：20
染色体と分子病態に基づくリスクに応じた
骨髄腫治療の層別化
座長：柴山 浩彦、黒田 純也
演者：Wee Joo Chng、知念 良顕、
金森 貴之、鈴木 一史

Pros and Cons
10：30－11：40
自家移植後の維持療法は必要か？どのような患者が適応で、どのような維持療法が良いのか？
座長：島崎 千尋、髙松 泰
演者：上村 智彦、尾崎 修治

12:00

ランチョンセミナー 1
12：00－12：50

Real-World Evidence and Clinical Implications
座長：柴山

浩彦

演者：Sundar Jagannath

セルジーン株式会社

ランチョンセミナー 2
12：00－12：50

新薬時代におけるprogression-free plateau
座長：鈴木

憲史

演者：太田

健介

ブリストル・マイヤーズ スクイブ株式会社

13:00

総会
13：10－13：40
プレシジョンメディシン時代における多発性骨髄腫治療の展望

会長講演
13：40－14：10

14:00

プレナリー 1
14：10－15：10

座長：中世古

15:00

知昭、服部

座長：村上
演者：飯田

演者：半田

座長：飯田 真介、張 高明
寛、Andrew Spencer、Saad Z. Usmani

ヤンセンファーマ株式会社 メディカルアフェアーズ本部
17:00

18:00

博和
真介

豊

スポンサードシンポジウム1
15：20－16：50
高齢多発性骨髄腫患者の治療

16:00

ポスター 1『多発性骨髄腫の分子病態 1』

座長：芦原 英司
ポスター 2『多発性骨髄腫の分子病態 2』
座長：花村 一朗
ポスター 3『多発性骨髄腫及び類縁疾患の検査法』

座長：渡辺 隆ポスター 4『多発性骨髄腫に対するトランスレーショナルリサーチ 1』
座長：今井 陽一ポスター 5『多発性骨髄腫に対するトランスレーショナルリサーチ 2』
座長：塚田 順一
ポスター 6『形質細胞性腫瘍の症例報告(診断・病理）』
座長：小杉 浩史
ポスター 7『多発性骨髄腫の症例報告(治療１）』
座長：佐々木 純
ポスター 8『多発性骨髄腫の症例報告(治療2）』
座長：八木 秀男
ポスター 9『骨髄腫類縁疾患の症例報告・新規治療法』

座長：堺田 惠美子ポスター 10『移植適応多発性骨髄腫の治療1』
座長：角南 一貴

19:00

全員懇親会
19：00－
名古屋マリオットアソシアホテル16階
20:00

14

閲覧
10：00－17：10

アイリス

ポスター発表17：10－18：30

5 月 12 日（日）
会場名

第1会場

第2会場

ポスター会場

部屋名

大ホール
（2F）

902
（9F）

展示場
（8F）

モーニングセミナー 1
8：00－8：40
カルフィルゾミブの持つ免疫学特性＝長期使用が可能なプロテアソーム阻害薬＝モーニングセミナー 2
8：00－8：40
多発性骨髄腫に対する免疫学的アプローチ

小野薬品工業株式会社

ブリストル・マイヤーズ スクイブ株式会社

8:00

座長：半田

寛

演者：伊藤

量基

座長：伊藤

薫樹

演者：萩原

將太郎

9:00

シンポジウム2
9：00－10：10
合併症の病態に基づく骨髄腫の最適な治療選択

10:00

座長：石田 禎夫、伊藤 薫樹
演者：Sundar Jagannath、淵田 真一、
安倍 正博

11:00

スポンサードシンポジウム2
10：20－11：50
多発性骨髄腫治療におけるMRDの意義
座長：宮本 敏浩
演者：Hervé Avet-Loiseau、髙松セルジーン株式会社閲覧
8：00－14：30

博幸

12:00

ランチョンセミナー 3
12：10－13：00
Unmet medical needs in maintenance treatment for
newly diagnosed multiple myeloma (NDMM)
座長：竹迫
13:00

直樹

演者：Wee Joo Chng

武田薬品工業株式会社

ランチョンセミナー 4
12：10－13：00
CD38の基礎知識を骨髄腫治療に応用する～ダラツムマブの効果を最大限に発揮するために～
座長：安倍

正博

演者：三原

圭一朗

ヤンセンファーマ株式会社

シンポジウム3
13：15－14：15
骨髄腫領域の診断および治療における技術革新
14:00

座長：安倍 正博、木崎 昌弘
演者：Andrew Spencer、藤原 弘、水野 晋一

15:00

16:00

プレナリー 2
16：00－17：00

座長：田村
17:00

秀人、半田

17：00－17：15

寛

閉会式

ポスター 11『移植適応多発性骨髄腫の治療2』
座長：塚田 信弘
ポスター 12『多発性骨髄腫の病態と疫学研究』
座長：和泉 透ポスター 13『治療法の研究（抗体療法）』
座長：林 敏昭
ポスター 14『治療法の研究（プロテアソーム阻害薬）』

座長：石川 隆之
ポスター 15『治療法の研究（レナリドミド・その他）』

座長：三木 浩和
ポスター 16『治療法の研究（ポマリドミド）』
座長：杉浦 勇ポスター 17『レジストリー研究と新規治療法の開発』

座長：河野 和ポスター 18『多発性骨髄腫の合併症・有害事象対策・診療支援１』

座長：若山 聡雄ポスター 19『多発性骨髄腫の合併症・有害事象対策・
診療支援２』

座長：磯田 淳

ポスター発表14：30－15：50

撤去
16：00－17：00

18:00

15

Schedule
Day 1: May 11, 2019
会場名

Room 1Room 2

Poster

部屋名

WINC HALL
（2F）

902
（9F）

Exhibition Space
（8F）

8:00

9:00

10:00

11:00

8:50 - 9:00 Opening Ceremony
Symposium 1
9:00 - 10:20
Treatment strategies based on the risk
catogories defined by choromosomal andmolecular alterations in MM

Put up Poster
8:30 - 10:00

Chairpersons: Hirohiko Shibayama, Jyunya Kuroda
Speakers: Wee Joo Chng,Yoshiki Chinen,
Takashi Kanamori, Kazuhito Suzuki

Pros and Cons
10:30 - 11:40
Is maintenance therapy after autologous stem celltransplantation necessary? If yes, who are the mostsuitable patients and what is the most suitable regimen?
Chairpersons: Chihiro Shimazaki, Yasushi Takamatsu
Speakers: Tomohiko Kamimura, Shuji Ozaki

12:00

Luncheon Seminar 1
12:00 - 12:50
Real-World Evidence and Clinical Implications
Chairperson: Hirohiko Shibayama Speaker: Sundar Jagannath【Celgene K.K.】

Luncheon Seminar 2
12:00 - 12:50
Progression-free plateau in era of new agents

Chairperson: Kenshi Suzuki Speaker: Kensuke Ohta
【Bristol-Myers Squibb Company】

13:00

General Assembly
13:10 - 13:40
14:00

Treatment of multiple myeloma in thisera of precision medicine: a perspective

Presidential Lecture
13:40 - 14:10

Chairperson: Hirokazu Murakami
Speaker: Shinsuke Iida

Plenary 1
14:10 - 15:10

15:00

16:00

Chairpersons: Chiaki Nakaseko, Yutaka Hattori

Sponsored Symposium 1
15:20 - 16:50
Treatment strategy of elderly multiple
myeloma patients

Chairperson: Shinsuke Iida, Takaaki Chou
Speakers: Hiroshi Handa, Andrew Spencer,
Saad Z. Usmani【Janssen Pharmaceutical K.K.】

17:00

18:00

Poster 1『Molecular pathogenesis in multiple
myeloma 1』
Chairperson: Eiji Ashihara
Poster 2『Molecular pathogenesis in multiple
myeloma 2』
Chairperson: Ichiro Hanamura
Poster 3『Laboratory test in mutiple myeloma
and its related disorders』
Chairperson: Takashi Watanabe
Poster 4『Translational research for multiple
myeloma 1』
Chairperson: Yoichi Imai
Poster 5『Translational research for multiple
myeloma 2』
Chairperson: Junichi Tsukada
Poster 6『Case reports: diagnosis andpathology in plasma cell neoplasms』
Chairperson: Hiroshi Kosugi
Poster 7『Case reports (1): treatment in
multiple myeloma』
Chairperson: Makoto Sasaki
Poster 8『Case reports (2): treatment in
multiple myeloma』
Chairperson: Hideo Yagi
Poster 9『Case reports: treatment with novel
therapy in myeloma-related disorders』
Chairperson: Emiko Sakaida
Poster 10『Stem-cell transplant in multiple
myeloma (1)』Chairperson: Kazutaka Sunami

19:00

Gala Dinner
19:00 Marriott Nagoya Associa 16F Iris
20:00

16

Poster viewing
10:00 - 17:10

Poster Session
17:10 - 18:30

Schedule
Day 2: May 12, 2019
会場名

Room 1Room 2

Poster

部屋名

WINC HALL
（2F）

902
（9F）

Exhibition Space（8F）

Morning Seminar 1
8:00 - 8:40

Morning Seminar 2
8:00 - 8:40

8:00

Focus on immunological characteristics behind Calfilzomib Immunological Apprcach for Multiple Myeloma
Chairperson: Hiroshi Handa Speaker: Tomoki Ito
Chairperson: Shigeki Ito Speaker: Shotaro Hagiwara【ONO PHARMACEUTICAL CO., LTD.】【Bristol-Myers Squibb Company】
9:00

Symposium 2
9:00 - 10:10
Optimal treatment choice for MM based on thepathogenesis of its complications
10:00

11:00

Chairpersons: Tadao Ishida, Shigeki Ito
Speakers: Sundar Jagannath, Shin-ichi Fuchida,
Masahiro Abe

Sponsored Symposium 2
10:20 - 11:50
Role of MRD Assessment in Multiple Myeloma

Chairperson: Toshihiro Miyamoto
Speakers: Hervé Avet-Loiseau, Hiroyuki Takamatsu

Poster viewing
8:00 - 14:30【Celgene K.K.】

12:00

Luncheon Seminar 3
Luncheon Seminar 4
12:10 - 13:00
12:10 - 13:00
Unmet medical needs in maintenance treatment for Apply required knowledge about CD38 for treatment in myeloma patients
newly diagnosed multiple myeloma (NDMM)～ To maximize the power of daratumumab for treatment ～13:00

Chairperson: Naoki Takezako Speaker: Wee Joo Chng
【Takeda Pharmaceutical Company Limited】

Symposium 3
13:15 - 14:15
Novel technological innovation in the field of
diagnosis and treatment of MM
14:00

Chairpersons: Masahiro Abe, Masahiro Kizaki
Speakers: Andrew Spencer, Hiroshi Fujiwara,
Shin-ichi Mizuno

15:00

16:00

Plenary 2
16:00 - 17:00

Chairpersons: Hideto Tamura, Hiroshi Handa
17:00

17:00 - 17:15

Closing Ceremony

Chairperson: Masahiro Abe Speaker: Keichiro Mihara【Janssen Pharmaceutical K.K.】

Poster 11『Stem-cell transplant in multiple
myeloma (2)』Chairperson: Nobuhiro Tsukada
Poster 12『Pathogenesis and epidemiologyof multiple myeloma』
Chairperson: Tohru Izumi
Poster 13『Monoclonal antibodies in multiple
myeloma』
Chairperson: Toshiaki Hayashi
Poster 14『Proteasome inhibitors in multiple
myeloma』
Chairperson: Takayuki Ishikawa
Poster 15『Lenalidomide and other treatment
modality in multiple myeloma』
Chairperson: Hirokazu Miki
Poster 16『Pomalidomide in multiple myeloma』
Chairperson: Isamu Sugiura
Poster 17『Registry data and novel therapy
in multiple myeloma』
Chairperson: Yawara Kawano
Poster 18『Complications, adverse events, andsupportive care in multiple myeloma (1)』Chairperson: Toshio Wakayama
Poster 19『Complications, adverse events, andsupportive care in multiple myeloma (2)』Chairperson: Atsushi Isoda

Poster Session
14:30 - 15:50

Poster Withdrawal
16:00 - 17:00

18:00

17

プログラム（Program）

プログラム（Program）

会長講演
5月11日㈯

13:40 - 14:10

座長：村上

PL

第1会場

博和（Hirokazu Murakami）（群馬大学大学院保健学研究科生体情報検査科学講座）

プレシジョンメディシン時代における多発性骨髄腫治療の展望
Treatment of multiple myeloma in this era of precision medicine: a perspective

飯田真介（Shinsuke Iida）

名古屋市立大学大学院医学研究科 血液・腫瘍内科学

シンポジウム1
5月11日㈯9:00 - 10:20

第1会場

染色体と分子病態に基づくリスクに応じた骨髄腫治療の層別化
Treatment strategies based on the risk catogories defined by choromosomal andmolecular alterations in MM
座長：柴山
黒田

SY1-1

浩彦（Hirohiko Shibayama）（大阪大学大学院 医学系研究科 血液・腫瘍内科）
純也（Jyunya Kuroda）（京都府立医科大学 血液内科）

Treatment strategy in high-risk multiple myeloma

Wee Joo Chng

National University Cancer Institute, Singapore

SY1-2

多発性骨髄腫の染色体・ゲノム診断の基礎と展望
Current standard and future perspective of cytogenetic and genetic diagnosis in
multiple myeloma

知念良顕（Yoshiki Chinen）

京都府立医科大学 血液内科

SY1-3

日本人新規診断多発性骨髄腫における網羅的ゲノム解析
Comprehensive genetic analysis of newly diagnosed multiple myeloma in Japan

金森

SY1-4

1,2
貴之
（Takashi Kanamori）
、眞田

昌 2、李

政樹 3、飯田

真介 3

1

2

名古屋市立大学大学院医学研究科 血液・腫瘍内科学、 国立病院機構名古屋医療センター 高度診断研究部、

3

名古屋市立大学大学院医学系研究科 血液・腫瘍内科学

多発性骨髄腫における染色体異常と治療戦略
Treatment strategy stratified with cytogenetic abnormality in multiple myeloma

鈴木一史（Kazuhito Suzuki）

東京慈恵会医科大学附属柏病院 腫瘍・血液内科

20

プログラム（Program）

5月12日㈰9:00 - 10:10

会長講演

シンポジウム2
第1会場

合併症の病態に基づく骨髄腫の最適な治療選択
座長：石田
伊藤

SY2-1

シンポジウムOptimal treatment choice for MM based on the pathogenesis of its complications
禎夫（Tadao Ishida）（日本赤十字社医療センター 血液内科）
薫樹（Shigeki Ito）
（岩手医科大学 臨床腫瘍学講座）

Therapeutic Strategies for Multiple Myeloma with Renal Impairment

Sundar Jagannath

Mount Sinai Hospital, New York, NY, USA

SY2-2アミロイドーシス合併骨髄腫患者の治療
Treatment of multiple myeloma complicated with AL amyloidosis

淵田真一（Shin-ichi Fuchida）

JCHO 京都鞍馬口医療センター 血液内科

SY2-3

骨髄腫骨病変治療の進歩と展望
Current status and future perspective of the treatment for myeloma bone disease

安倍正博（Masahiro Abe）

徳島大学大学院医歯薬学研究部 血液・内分泌代謝内科学分野

シンポジウム3
5月12日㈰13:15 - 14:15

第1会場

骨髄腫領域の診断および治療における技術革新
Novel technological innovation in the field of diagnosis and treatment of MM
座長：安倍
木崎

SY3-1

正博（Masahiro Abe）
（徳島大学大学院 医歯薬学研究部 血液・内分泌代謝内科学）
昌弘（Masahiro Kizaki）（埼玉医科大学総合医療センター 血液内科）

Andrew Spencer
Department of Clinical Haematology, Alfred Hospital, Melbourne, Australia

SY3-2

骨髄腫関連腫瘍抗原を認識する受容体遺伝子を導入した T 細胞を用いる治療抵抗性骨髄腫に対する養子免疫療法

Adoptive cellular immunotherapy against refractory myeloma using engineered T cells
to express receptor for myeloma-associated tumor antigen

藤原弘（Hiroshi Fujiwara）

三重大学大学院医学系研究科 個別化がん免疫治療学分野

SY3-3

造血器腫瘍のプレシジョンメディシン：多発性骨髄腫における現状とこれから
Precision medicine in hematological malignancies: current status in multiple myeloma

水野晋一（Shinichi Mizuno）

九州大学 医学研究院保健学部門検査技術学分野

21

プログラム（Program）

Pros and Cons
5月11日㈯

10:30 - 11:40

第1会場

自家移植後の維持療法は必要か？どのような患者が適応で、どのような維持療法が良いのか？
Is maintenance therapy after autologous stem cell transplantation necessary? If yes,
who are the most suitable patients and what is the most suitable regimen?
座長：島崎
髙松

PC-1

千尋（Chihiro Shimazaki）（独立行政法人 地域医療機能推進機構京都鞍馬口医療センター 血液内科）
泰（Yasushi Takamatsu）（福岡大学 腫瘍血液感染症内科）

自家移植後の維持療法は行うべきである
Maintenance therapy is necessary for patients with MM following ASCT上村

智彦
（Tomohiko Kamimura）

原三信病院 血液内科

PC-2

自家移植後の維持療法は全例に必要か？
Should all patients receive maintenance therapy after autologous stem celltransplantation?

尾崎修治（Shuji Ozaki）

徳島県立中央病院 血液内科

22プログラム（Program）

プレナリー 1
5月11日㈯

14:10 - 15:10

第1会場

座長：中世古 知昭（Chiaki Nakaseko）（国際医療福祉大学医学部 血液内科）
服部 豊（Yutaka Hattori）（慶應義塾大学薬学部 病理生理学講座）

PL1-1

Phase 3 Study of Daratumumab Plus Lenalidomide and Dexamethasone (D-Rd) Vs. Rd
in Transplant-ineligible Newly Diagnosed Multiple Myeloma (NDMM): MAIA

Saad Usmani1、Shaji K. Kumar 2、Torben Plesner3、Robert Z. Orlowski4、Philippe Moreau5、Nizar Bahlis6、Supratik Basu7、Hareth Nahi8、Cyrille Hulin9、Hang Quach10、Pros and Cons

Hartmut Goldschmidt11、Michael O’Dwyer12、Aurore Perrot13、Christopher P. Venner14、Katja Weisel15、Joseph R. Mace16、Tahamtan Ahmadi17、Christopher Chiu18、Jianping Wang19、Rian van Rampelbergh20、Clarissa M. Uhlar18、Rachel Kobos19、Ming Qi18、Thierry Facon21
1

Levine Cancer Institute/Atrium Health, Charlotte, NC, USA、2Department of Hematology, Mayo Clinic

Rochester, Rochester, MN, USA、3Vejle Hospital and University of Southern Denmark, Vejle, Denmark、
Department of Lymphoma and Myeloma, University of Texas M.D. Anderson Cancer Center, Houston, TX, USA、

5

Hematology, University Hospital Hôtel-Dieu, Nantes, France、6University of Calgary, Arnie Charbonneau

Cancer Institute, Calgary, AB, Canada、7Royal Wolverhampton Hospitals NHS Trust, Wolverhampton, United
Kingdom、8Karolinska Institute, Department of Medicine, Division of Hematology, Karolinska University
Hospital at Huddinge, Stockholm, Sweden、9Department of Hematology, Hospital Haut Leveque, University
Hospital, Pessac, France、10St. Vincent's Hospital, University of Melbourne, Melbourne, Australia、11University
Hospital Heidelberg and National Center of Tumor Diseases (NCT), Heidelberg, Germany、12Dept. of
Medicine/Haematology, NUI, Galway, Ireland、13Hematology Department, University Hospital, Vandoeuvre Les
Nancy, France、14Division of Medical Oncology University of Alberta, Edmonton, AB, Canada、
15

Universitaetsklinikum Tuebingen der Eberhard-Karls-Universitaet, Abteilung fuer Innere Medizin II,

Tuebingen, Germany、16Florida Cancer Specialists & Research Institute, St. Petersburg, FL, USA、17Genmab US,
Inc., Princeton, NJ, USA、18Janssen Research & Development, Spring House, PA, USA、19Janssen Research &Development, Raritan, NJ, USA、20Janssen Research & Development, Beerse, Belgium、21Service des Maladies
du Sang, Hôpital Claude Huriez, Lille, France

PL1-2

多発性骨髄腫における有糸分裂チェックポイントタンパク BUB1 高発現の機能的意義
Functional significance of Mitotic Checkpoint Protein BUB1 Overexpression in Multiple
Myeloma藤林

1
悠人（Yuto Fujibayashi）、坂元 - 稲田

黒田

純也

西山

1

PL1-3

大地 、松村 - 木元
11

弥生 、知念1

奈津美 1、桑原 - 太田

良顕 、志村1

沙絵子 1、伊佐勇司 、古林1

勉 、谷脇1

怜子 1、山口
雅史 、
2

順子 1、

京都府立医科大学大学院医学研究科 血液内科学、2 京都府立医科大学大学院分子診断・治療センター

多発性骨髄腫細胞で小胞体ストレス下において発現する CD98 は抗体療法の特異的標的となる

CD98 turns into a specific therapeutic target under endoplasmic reticulum stress in
multiple myeloma

長谷川

加奈（Kana Hasegawa）、保仙直毅

大阪大学大学院 医学系研究科 癌幹細胞制御学寄附講座

23

プレナリー１

4

プログラム（Program）
PL1-4

未治療多発性骨髄腫における末梢血 cell free DNA 解析
Analysis of serum cell free DNA in patients with multiple myeloma

立田

1
卓登
（Takuto Tachita）
、李

飯田

真介 1

木下

1

PL1-5

史緒理 、浅尾1

優 、成田1

政樹 1、青木朋子 、正木1

奨 1、浅野彩子 、伊藤2

有彩 1、金森旭 、楠本1

貴之 1、戸谷

茂 、小松
1

治仁 1、

弘和 1、

名古屋市立大学大学院医学研究科 血液・腫瘍内科学、2 名古屋市立大学大学院医学研究科 臨床病態病理学

造血幹細胞移植後の初発の多発性骨髄腫患者におけるイキサゾミブ維持療法による無増
悪生存期間の延長：TOURMALINE MM3 試験

Ixazomib Maintenance Post-Transplant Significantly Prolongs Progression-Free
Survival in Newly Diagnosed Multiple Myeloma: The TOURMALINE-MM3 Trial

Wee-Joo Chng1、Meletios A Dimopoulos2、Francesca Gay3、Fredrik H Schjesvold4、Meral Beksac5、Roman Hajek6、Katja C Weisel7、Hartmut Goldschmidt8、Vladimir Maisnar9、Philippe Moreau10、

Chang Ki Min11、Agnieszka Pluta12、Martin Kaiser13、Sonja Zweegman14、Maria Victoria Mateos15、Andrew Spencer16、Shinsuke Iida17、Gareth J Morgan18、Kaveri Suryanarayan19、

Zhaoyang Teng20、Tomas Skacel21、Antonio Palumbo21,22、Ajeeta B Dash23、Neeraj Gupta24、Richard Labotka19、S Vincent Rajkumar25

1Department of Haematology-Oncology, National University Cancer Institute, National University Health System,

Singapore, and Cancer Science Institute of Singapore, National University of Singapore, Singapore、
2

Hematology and Medical Oncology, Department of Clinical Therapeutics, National and Kapodistrian Universityof Athens, School of Medicine, Athens, Greece、3Department of Oncology and Hematology, Azienda
Ospedaliero-Universitaria City of Health and Science of Turin, Turin, Italy、4Oslo Myeloma Center, Oslo
University Hospital, Oslo, Norway, and KG Jebsen Center for B cell malignancies, University of Oslo, Oslo,
Norway、5Department of Hematology, Ankara University, Ankara, Turkey、6Department of Hematooncology,
University Hospital Ostrava, Ostrava, Czech Republic、7Department of Internal Medicine II, University Hospital
Tübingen, Tübingen, Germany、8Department of Internal Medicine V, University Medical Hospital Heidelberg
and National Center of Tumor Diseases, Heidelberg, Germany、9Fourth Department of Medicine – Hematology,
University Hospital Hradec Králové, Hradec Králové, Czech Republic、10Department of Hematology, University
Hospital Hôtel-Dieu, Nantes, France、11Department of Internal Medicine, Seoul St. Mary's Hospital, Seoul, South
Korea、12Department of Hematology, Medical University of Lodz, Multidisciplinary Provincial Centre ofTraumatology and Oncology Nicolas Copernicus in Lodz, Lodz, Poland、13Department of Haematology, The
Royal Marsden Hospital, London, UK, and Division of Molecular Pathology, The Institute of Cancer Research
ICR, London, UK、14Department of Hematology, Amsterdam University Medical Center, VU University
Amsterdam, Cancer Center Amsterdam, Amsterdam, Netherlands、15Department of Hematology, University
Hospital of Salamanca, CIC, IBMCC, Salamanca, Spain、16Malignant Haematology and Stem Cell Transplantation
Service, Alfred Health-Monash University, Melbourne, VA, Australia、17Department of Hematology andOncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan、18Myeloma Institute,
University of Arkansas for Medical Sciences, Little Rock, AR, USA、19Oncology Clinical Research, Millennium
Pharmaceuticals, Inc., a wholly owned subsidiary of Takeda Pharmaceutical Company Limited, Cambridge, MA,
USA、20Biostatistics, Millennium Pharmaceuticals, Inc., a wholly owned subsidiary of Takeda Pharmaceutical
Company Limited, Cambridge, MA, USA、21Global Medical Affairs, Millennium Pharmaceuticals, Inc., a wholly
owned subsidiary of Takeda Pharmaceutical Company Limited, Cambridge, MA, USA、22Myeloma Unit, Divisionof Hematology, University of Torino, Azienda Ospedaliero-Universitaria S Giovanni Battista, Turin, Italy, andCenter for Hematology and Oncology, University Hospital Zürich, Zürich, Switzerland、23Translational
Medicine, Millennium Pharmaceuticals, Inc., a wholly owned subsidiary of Takeda Pharmaceutical Company
Limited, Cambridge, MA, USA、24Drug Metabolism and Pharmacokinetics, Millennium Pharmaceuticals, Inc., awholly owned subsidiary of Takeda Pharmaceutical Company Limited, Cambridge, MA, USA、25Division of
Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA

24

プログラム（Program）

プレナリー 2
5月12日㈰16:00 - 17:00

座長：田村
半田

PL2-1

第1会場

秀人（Hideto Tamura）（日本医科大学 血液内科）
寛（Hiroshi Handa）（群馬大学大学院医学系研究科 血液内科学）

多発性骨髄腫における骨髄由来抑制系細胞誘導の分子メカニズムに対する IMiDs の効果
Potency of immunomodulatory drugs in interfering molecular mechanisms underlying
the induction of myeloid-derived suppressor cell in multiple myeloma

太田

藤林

堀池
1

悠人 1、下村重夫 1、谷脇とも子 1、水野雅史 2、黒田勇司 1、伊佐芳美 1、木元怜子 1、山口

弥生 1、塚本純也 1

順子 1、西山拓 1、知念大地 1、

良顕 1、古林

勉 1、

京都府立医科大学大学院医学研究科 血液内科学、2 京都府立医科大学大学院分子診断・治療センター

免疫調節薬は骨髄腫細胞の PD-L1 発現誘導により T 細胞抑制するが、durvalumab との併用で解除できる

Immunomodulatory drug-induced T-cell suppression via PD-L1 upregulation on
myeloma cells is recovered by durvalumab

石橋
1

PL2-3

秀人 3

淳一 2、伊藤拓水 2、半田宏 2、猪口孝一 3、

プレナリー２田村

1
真理子（Mariko Ishibashi）、山本

日本医科大学微生物学・免疫学、2 東京医科大学ナノ粒子先端医学部講座、3 日本医科大学血液内科

Connect® MM registry: Impact of initial treatment on HRQoL and outcomes in newly
diagnosed multiple myeloma without intent for immediate transplant:

Rafat Abonour1、Robert M Rifkin2、Cristina Gasparetto3、Kathleen Toomey4、Brian G. M. Durie5、James W. Hardin6、Howard R. Terebelo7、Sundar Jagannath8、Mohit Narang9、Sikander Ailawadhi10、Shankar Srinivasan11、Liang Liu11、Amani Kitali11、Amit Agarwal11、
Lynne Wagner12
1

Indiana University, Indianapolis, IN, USA、2Rocky Mountain Cancer Centers US Oncology, Denver, CO, USA、3

Duke University Medical Centre, Durham, NC, USA、4Steeplechase Cancer Center, Somerville, NJ, USA、

5

Cedars-Sinai Medical Center, Los Angeles, CA, USA、6University of South Carolina, Columbia, SC, USA、

7

Providence Cancer Institute, Novi, MI, USA、8Mount Sinai Hospital, New York, NY, USA、9US Oncology

Research, Columbia, MD, USA、10Mayo Clinic, Jacksonville, FL, USA、11Celgene Corporation, Summit, NJ, USA、
12

Wake Forest School of Medicine, Winston-Salem, NC, USA

PL2-4

新規薬剤時代における 65 歳以上骨髄腫の自家造血幹細胞移植の安全性と有効性：JSHCT

MM WG study

Efficacy and safety of autologous stem cell transplantation in elderly patients withmultiple myeloma in the era of novel agents: JSHCT MM WG study

水野

1
昌平
（Shohei Mizuno）、河村

神田

善伸 、一戸飯田

真介 6、中澤2

英之 7、牧田

辰夫 、熱田11

浩二 2、花村雅典 3、賀古由子

12,13

一朗 1、角南一貴 3、森博幸 、高見昭良

真一 2、澤、高松14

正史 8、上田1

毅彦 4、中村

恭典 9、髙橋

文彦 5、

寛行 10、

1

2

愛知医科大学 血液内科、 自治医科大学付属さいたま医療センター 血液科、3 岡山医療センター 血液内科、

4

慶應義塾大学医学部 血液内科、5 国立国際医療研究センター 血液内科、6 名古屋市立大学病院 血液・腫瘍内科、

7

信州大学医学部附属病院 血液内科、8 安城更生病院 血液・腫瘍内科、9 倉敷中央病院 血液内科、

10

横浜市立大学附属病院 血液内科、11 広島大学原爆放射線医科学研究所 血液・腫瘍内科、

12

日本造血細胞移植データセンター、13 名古屋大学大学院医学系研究科 医療行政学、

14

金沢大学 医薬保健研究域医学系血液・呼吸器内科

プレナリー１

PL2-2

1
沙絵子
（Saeko Kuwahara-Ota）、志村25

プログラム（Program）
PL2-5

多発性骨髄腫患者における腎機能回復の予測因子
The predictive factor of renal recovery in the patients with multiple myeloma

小林
北舘

宏紀
（Hiroki Kobayashi）
、寺尾
明宏、竹内

正美、末永

孝生

俊紀、津島

隆史、安部

佳亮、三浦

大典、成田

健太郎、

亀田総合病院 血液腫瘍内科

ポスター 1
5月11日㈯

17:10 - 18:30

ポスター会場多発性骨髄腫の分子病態

１

Molecular pathogenesis in multiple myeloma 1
座長：芦原

P1-1

英司（Eiji Ashihara）（京都薬科大学 病態生理学分野）

正常 B リンパ球由来 iPS 細胞を用いた多発性骨髄腫の発生機序の解明に向けて
Attempt to elucidate the mechanism of development of multiple myeloma using iPS
cells derived from normal B cells

坂井

1
晃（Akira Sakai）、柳池添隆之 5、小野寺太田

亜希 1、津山明伸 、Sivasundaram Karnan 、重村
2

2

雅史 6

尚宏 1、菅井倫成 、笹谷3

美咲 1、阿部悠 1、柳井めぐみ 、神谷4

祐佳理 1、

研二 、花村4

一朗 2、

1

福島県立医科大学医学部 放射線生命科学講座、2 愛知医科大学 血液内科学講座、3 信州大学医学部 小児科学講座、

4

広島大学 原医研 分子発がん制御、5 福島県立医科大学医学部 血液内科学講座、6 国立成育医療研究センター

成育遺伝研究部㊝ P1-2 Hexokinase-2(HK2) は低酸素誘導性オートファジーを制御し骨髄腫細胞のプロテアソー
ム阻害薬耐性に寄与する

Hexokinase-2 (HK2) regulates hypoxia-induced autophagy, leading to resistance ofproteasome inhibitor of multiple myeloma

池田
1

1
翔
（Sho Ikeda）、阿部

史人 1、北舘明宏 1,2、小林敬宏 1、髙橋

直人 1、田川博之 1

秋田大学医学部 血液・腎臓・膠原病内科、2 亀田総合病院 血液・腫瘍内科

P1-3 多発性骨髄腫の微小環境は可溶型 SLAMF7 以外の要因によって樹状細胞において Th1 誘導を抑制し Th2 誘導を増強する

Myeloma cells have the ability to suppress Th1-inducing capacity but enhance Th2mediated response of DCs by factors other than soluble SLAMF7

東由子（Yoshiko Azuma）
、伊藤

堀田

雅章、中西

孝尚、藤田

量基、重坂

真也、佐竹

実、今井

敦、中谷

開、斎藤

綾、宮地

陵、小西

理彦、石井

晶子、吉村

一慶、野村

英晃、

昌作

関西医科大学第一内科学講座

P1-4 多発性骨髄腫において NOTCH1 と JAG1 の相互作用が増悪化を誘導する
The interaction of NOTCH1 with JAG1 induces aggressive myeloma behavior

上田

26

1
圭馬
（Keima Ueda）、石橋2

真理子 2、今井

陽一 3、猪口3

孝一 4、田村秀人 41

日本医科大学医学部 5 学年、 日本医科大学微生物学・免疫学、 東京大学医科学研究所附属病院血液腫瘍内科、

4

日本医科大学血液内科

プログラム（Program）
P1-5 血清 KL-6 値は多発性骨髄腫の予後予測因子となりうる
KL-6 may be an excellent predictor of prognosis in multiple myeloma

砂川

半田

小松

1
実香
（Mika Sunakawa）、
石橋

寛 、佐々木3

則夫 4、猪口純 、今井真理子 2、海渡

陽一 、田中4

孝一 1、田村裕太 1、木下紀奈 、伊藤5

秀人 1

6

量介 1、朝山薫樹 、田野崎7

敏夫 1、守屋

栄 、田中
8

1

日本医科大学 血液内科、 日本医科大学 微生物学・免疫学、3 群馬大学医学部附属病院 血液内科、

4

順天堂大学医学部順天堂医院 血液内科、5 東京大学医科学研究所、6 東京女子医科大学 血液内科、

7

岩手医科大学 臨床腫瘍学講座、8 同愛記念病院 血液内科

慶一 1、

淳司 6、

2

ポスター 2
5月11日㈯

17:10 - 18:30

ポスター会場多発性骨髄腫の分子病態

２

Molecular pathogenesis in multiple myeloma 2
座長：花村一朗（Ichiro Hanamura）（愛知医科大学 血液内科）㊝ P2-1 多発性骨髄腫細胞における低酸素適応のための exosome 分泌過多戸田侑紀（Yuki Toda）、中山

紗矢香、細木誠之、芦原

プレナリー２

Increased exosome secretion is a way of hypoxic adaptation in multiple myeloma cells
英司

京都薬科大学薬学部 病態生理学分野

P2-2 不動は骨吸収と骨髄腫進展を促進させる
谷本

1,2
幸多朗
（Kotaro Tanimoto）、日浅中村

信元 2、三木Mohannad Ashtar 、小田1

1,2

明日香 、岩佐2

浩和 5、遠藤雅博 1,2、天真

寛文 1,2、寺町

昌美 、曾我部逸朗 4、田中2

公子 、大浦栄二 1、松本2

順平 2,3、

雅弘 2、原田俊夫 6、安倍

正博 2

ポスター１

Immobilization promotes bone resorption and tumor expansion in myeloma
武志 2、

2

徳島大学大学院 医歯薬学研究部 口腔顎顔面矯正学分野、 徳島大学大学院 医歯薬学研究部
ポスター２

血液・内分泌代謝内科学分野、3 徳島大学大学院 医歯薬学研究部 組織再生制御学、4 徳島大学大学院
医歯薬学研究部 生体機能解析学分野、5 徳島大学病院 輸血・細胞治療部、6 徳島大学 藤井節郎記念医科学センター

P2-3 骨髄腫細胞間相互作用による薬剤耐性獲得機構の解明
The role of myeloma cell homophilic interaction in drug resistance菊池㊝ P2-4

1
次郎（Jiro Kikuchi）、長田

直希 1、小山大輔 1、黒田芳明 2、安井

寛 3、古川1

自治医科大学分子病態治療研究センター 幹細胞制御研究部、2 広島西医療センター内科、

3

東京大学医科学研究所

祐雄 1

ROS の骨髄腫の骨病変と癌治療関連骨減少症の誘発における重要な役割
Critical roles of ROS in induction of bone disease and cancer treatment-induced boneloss in myeloma

Mohannad Ashter1、天真
岩佐

三木
1

昌美 4、原田

浩和 、田中5

寛文 2、寺町

武志 4、藤井栄二 、松本2

順平 3、日浅志朗 4、香川俊夫 、安倍6

雅博 2、谷本

久美子 4、大浦正博

4

幸多朗 1、小田雅博 4、曽我部明日香 4、

公子 4、中村

信元 4、

徳島大学大学院 口腔科学教育部 口腔顎顔面矯正学分野、2 徳島大学大学院 医歯薬学研究部

口腔顎顔面矯正学分野、3 徳島大学大学院 医歯薬学研究部 組織再生制御学、4 徳島大学大学院 医歯薬学研究部
血液・内分泌代謝内科学分野、5 徳島大学病院 輸血・細胞治療部、6 徳島大学 藤井節郎記念医科学センター

27

プログラム（Program）
P2-5 多発性骨髄腫細胞サブセットに対する腫瘍免疫の応答予測
Response prediction and mechanisms of tumor immunosurveillance against multiple
myeloma cell subsets

八幡

1,2
真人
（Makoto Yawata）、Siti Sarah Daud1、Ryo Takahashi1、Ankurina Sharma1、Sathish Gopalakrishnan3、Kiat Hoe Ong4、八幡

信代 5、Wee Joo Chng6

1

Department of Pediatrics, National University of Singapore and National University Health System, Singapore、

2Singapore Institute for Clinical Sciences, Agency for Science Technology and Research, Singapore、

3

Department of Haematology, Singapore General Hospital, Singapore、4Department of Haematology, Tan Tock

Seng Hospital, Singapore、5Department of Ophthalmology, Kyushu University、6Department of
Haematology-Oncology, National University of Singapore and National University Health System, Singapore

ポスター 3
5月11日㈯

17:10 - 18:30

ポスター会場多発性骨髄腫及び類縁疾患の検査法
Laboratory test in mutiple myeloma and its related disorders
座長：渡辺隆（Takashi Watanabe）（三重大学大学院医学系研究科 遺伝子・免疫細胞治療学）

P3-1 多発性骨髄腫 MRD 検出における SRL 8 カラー・1 チューブ MFC と EuroFlow-NGF の比較
Comparison of MRD detection in multiple myeloma between SRL 8-color single-tube
and EuroFlow 8-color 2-tube multiparameter flow cytometry methods

高松

村田
1

1
博幸
（Hiroyuki Takamatsu）、鎧高

了一 3、上田幹夫 3、中尾

健志 1、藤澤眞二 1、末永孝生 4

桃子 1、小堀一弥 2、塙

正子 2、山下剛史 3、2

金沢大学 血液・呼吸器内科、 株式会社エスアールエル、3 恵寿金沢病院 内科、4 亀田総合病院

血液・腫瘍内科

P3-2 VS38 はダラツムマブ使用下でも CD38 に代わり形質細胞を検出し得る有用な抗体である
VS38 as a promising CD38 substitute antibody for flow cytometric detection of plasma
cells in the daratumumab era

河田

木場

1,2
岳人
（Takahito Kawata）、
水田悠介 1、右京直哉 1、為金

駿平 3,4、川畑

現 1、渡邊

光正 1

宏志 3、山根範子 3、物延

沙耶 3、駒井1

兵庫県立尼崎総合医療センター 血液内科、 京都大学大学院医学研究科 血液・腫瘍内科学、3

兵庫県立尼崎総合医療センター 検査部、4 神戸大学大学院保健学研究科 病態解析学領域

隆夫 3、

2

P3-3 10color-MFC の基礎検討
Basic study of Multiparameter flow cytometry

坂本

1
淳（Jun Sakamoto）、石田

宇藤

唯 2、余語塚田

1

28

信弘 、岡塚2

貴世志 、阿部2

孝夫 2、梨本禎夫 2、野間有 、吉識2

淳一郎 2、鈴木2

芳弘 1、金子由実子 、宮崎2

憲史 2

成人 1、前田寛至 、佐藤2

株式会社ビー・エム・エル 細胞性免疫課、 日本赤十字社医療センター 血液内科

亜希 1、浜崎

広太 、小倉
2

博行 1、

瑞生 2、

プログラム（Program）
P3-4 骨髄腫臨床検体バンクの構築およびクローナリティ解析についての進捗報告
Establishment of clinical myeloma specimen bank and progress report of clonality
analysis

竹下

工藤
1

1,2
昌孝
（Masataka Takeshita）、小玉

大輔 1、三輪信之 2、平井哲義 1,2

理泉 1、谷村

聡 1、岡崎幸治 1、奥田

優子 1、

地域医療振興協会 東京北医療センター 血液内科、2 国際骨髄腫先端治療研究センター

P3-5 NGS による AL アミロイドーシスでのクローナル免疫グロブリンλ遺伝子の同定
Identification of clonal immunoglobulin λ light-chain gene rearrangements in AL
amyloidosis by next generation sequencing

木村

1
賢司
（Kenji Kimura）、塚本

武内

正博 、大和田

Rahmutulla Bahityar4、福世1

中世古

知昭 6、堺田祥吉 1、宮崎真樹 4、大島 ( 長谷川 )

千桂子 、井関
1

惠美子 1

徹

、松坂

1,5

寛至 2、真子 ( 川尻 )渚 1、三川恵介 、金田4

千華 3、

紫緒 1,5、竹田

篤志 、石田4

勇輔 1、三村禎夫 、鈴木2

尚也 1,5、

憲史 2、

1

千葉大学医学部附属病院 血液内科、2 日本赤十字医療センター 血液内科、3 大網白里市立国保大網病院、

4

千葉大学大学院医学研究院 分子腫瘍学、5 千葉大学医学部附属病院 輸血・細胞療法部、

6

国際医療福祉大学医学部 血液内科

ポスター 4
5月11日㈯

17:10 - 18:30

ポスター会場多発性骨髄腫に対するトランスレーショナルリサーチ

１

Translational research for multiple myeloma 1
座長：今井陽一（Yoichi Imai）（東京大学医科学研究所附属病院 血液腫瘍内科）

P4-1 多発性骨髄腫に対する新規 CAR T 細胞療法の開発
Development of a novel CAR T-cell therapy for multiple myeloma
直毅（Naoki Hosen）

ポスター２

保仙

大阪大学大学院医学系研究科 癌幹細胞制御学

P4-2 骨髄腫細胞における PBZ binding kinase の腫瘍促進作用と治療標的分子としての可能性

太田
1

1
明伸
（Akinobu Ota）
、花村

一朗 2、Sivasundaram Karnan1、高見昭良 2、細川

ポスター３

Role of PBK in multiple myeloma cell growth: implication of PBK in novel moleculartargets for anti-myeloma therapy
好孝 12

愛知医科大学 医学部生化学講座、 愛知医科大学 医学部血液内科学講座

P4-3 温熱療法による骨髄腫細胞の TRAIL 感受性の亢進

三木

寺町
原田

1
浩和
（Hirokazu Miki）、中村

順平 4、岡本

武志 、藤井2

恵暢 2、大浦

志朗 、賀川2

信元 2、Ariunzaya Bat-Erdene2、天真

雅博 2、曽我部久美子 、安倍2

公子 2、髙橋
正博

2

寛文 3、小田真美子 2、岩佐昌美 2、宇髙明日香 2、
憲吾 2、

1

徳島大学病院 輸血・細胞治療部、2 徳島大学大学院医歯薬学研究部 血液・内分泌代謝内科学、

3

徳島大学大学院医歯薬学研究部 口腔顎顔面矯正学分野、4 徳島大学大学院医歯薬学研究部 口腔組織学分野

29

ポスター４

Sensitization of myeloma cells to a TRAIL-mediated immunotherapy withhyperthermia

プログラム（Program）㊝ P4-4 HDAC1-IRF4-PIM2 経路を標的とする新規抗骨髄腫療法の開発
The novel therapeutic strategy targeting the HDAC1-IRF4-PIM2 pathway in myeloma
cells

原田

1
武志
（Takeshi Harada）
、小田

曽我部

公子 1、岩佐昌美 2、藤井Anderson Kenneth 、安倍
1

6

正博

2

明日香 2、天眞

志朗 2、中村

寛文 3、寺町

信元 2、三木順平 4、大浦浩和 5、賀川雅博 1、久美子 1、秀島輝 6、

徳島大学病院 血液内科、2 徳島大学大学院 医歯薬学研究部 血液・内分泌代謝内科学、3 徳島大学大学院

医歯薬学研究部 口腔顎顔面矯正学、4 徳島大学大学院 医歯薬学研究部 組織再生制御学、5 徳島大学病院
輸血・細胞治療部、6 ハーバード大学医学部 ダナ・ファーバー癌研究所

P4-5 形質細胞特異的な代謝関連分子を標的とした多発性骨髄腫の治療開発研究
Targeting AMPD1, a plasma cell specific metabolic molecule, for multiple myeloma
treatment

河野1
和（Yawara Kawano）
、稲田

松岡

1

雅雄

優紀 2、笹野1

孝行 2、西村

直 1、松下

豊 2、畑

裕之 2、

熊本大学医学部附属病院 血液・膠原病・感染症内科、2 熊本大学生命科学研究部生体情報解析学分野

ポスター 5
5月11日㈯

17:10 - 18:30

ポスター会場多発性骨髄腫に対するトランスレーショナルリサーチ

２

Translational research for multiple myeloma 2
座長：塚田順一（Junichi Tsukada）（産業医科大学病院 血液内科）

P5-1 骨髄腫細胞に対する新規 PDK1 阻害剤 JX06 の有用性
JX06, a potent and selective PDK1 inhibitor, is highly promising in myeloma
therapeutic strategy

笹野
1

1
孝行
（Takayuki Sasano）、河野

和 2、松下豊 1、松岡雅雄 2、畑裕之 1

2

熊本大学 保健学教育部 生命科学研究部生体情報解析学分野、 熊本大学医学部附属病院

血液・膠原病・感染症内科㊝ P5-2 多発性骨髄腫治療抵抗性のバイオマーカーの探索
Establishment of diagnostic biomarkers for the relapsed/refractory multiple myeloma
in patients treated with lenalidomide-based therapies

小林

佐々木

1
真之
（Masayuki Kobayashi）
、安井

純 、川俣
6

豊隆 、牧山2

寛 2、佐藤純也 、横山2

広太 3、石田

和明 、東條
2

禎夫 3、田村

有伸

、今井

1,2

秀人 4、半田

陽一

2

寛 5、

1

2

東京大学医科学研究所 分子療法分野、 東京大学医科学研究所附属病院 血液腫瘍内科、

3

日本赤十字社医療センター 血液内科、4 日本医科大学 血液内科、5 群馬大学 血液内科、6 順天堂大学 血液内科

㊝ P5-3 骨髄腫治療における Akt 阻害と PRC2 阻害の相乗効果
Akt Inhibition Synergizes with PRC2 inhibition in the treatment of Multiple Myeloma

Mohamed Rizk1,2、Ola Rizq2、大島

三村

30

尚也 3

基彦 1,2、中島やえ子 1,2、一色佑介 2、岩間厚志 1,2、

1

東京大学医科学研究所 幹細胞治療研究センター 幹細胞分子医学、2 千葉大学大学院医学研究院 細胞分子医学、3

千葉大学医学部附属病院 輸血・細胞療法部

プログラム（Program）
ポスター６

P5-4 多発性骨髄腫における新規多価ペプチドワクチン PVX-410, PVX-024 の開発
Development of novel, multi-peptide-based cancer vaccine PVX-410 and PVX-024 formultiple myeloma

安井

1
寛（Hiroshi Yasui）、東條

Kenneth Anderson2

1

有伸 1、Jooeun Bae2、Doris Peterkin3、Nikhil Munshi2、

東京大学医科学研究所 附属病院血液腫瘍内科、2Dana-Farber Cancer Institute, Harvard Medical School, MA,

USA、3OncoPep Inc., MA, USA

P5-5 新規フタルイミド体 TC11 はチューブリン重合阻害および MCL1 分解を介してセレブロ
ン非依存的に骨髄腫細胞のアポトーシスを導く

A novel phenylphthalimide, TC11, inhibits tubulin polymerization and degrades MCL1
followed by apoptosis of myeloma cells without modulating cereblon

大澤

藤橋
1

1
翔
（Sho Osawa）、
市川

和也 、松下1

大樹 1、中村

麻衣子 、柳川1

美沙 1、室田

弘志 、服部2

豊1

若菜 1、不藤

拓海 1、辻宏樹 1、佐俣光一 1、

2

慶應義塾大学薬学部、 IDAC セラノスティクス株式会社

ポスター 6
5月11日㈯

17:10 - 18:30

ポスター会場

形質細胞性腫瘍の症例報告(診断・病理）
Case reports: diagnosis and pathology in plasma cell neoplasms
座長：小杉浩史（Hiroshi Kosugi）（大垣市民病院 血液内科）

P6-1 多発性骨髄腫の経過中に発症し形質細胞腫との鑑別に苦慮した形質細胞様型浸潤性尿路上皮癌

Metastatic plasmacytoid urothelial carcinoma mimicking plasmacytoma in a patientwith multiple myeloma

飯塚

1,2
弘子
（Hiroko Iiduka）、岩尾

憲明 2、小池

道明 2、野口雅章 1、小松1

順天堂大学医学部附属浦安病院 血液内科、2 順天堂大学医学部附属静岡病院 血液内科、

3

順天堂大学医学部内科学血液学講座

則夫 3

P6-2 IgA 血管炎の経過中に発症した Plasmablastic plasma cell myeloma の一例
A case of plasmablastic plasma cell myeloma developed during IgA vasculitis
treatment

鈴木

利貴央（Rikio Suzuki）
、川井

英嗣、古谷

大輔、小川

吉明、川田

浩志、安藤

潔

東海大学医学部 血液・腫瘍内科

ポスター４

P6-3 閉塞性黄疸を合併し、胆管癌を疑われた形質細胞腫の 1 例
A case of plasmacytoma suspected of cholangiocarcinoma complicated by obstructive
jaundice

金杉丈（Jo Kanasugi）
、加藤

千絵、伊藤

公人

大同病院 血液・化学療法内科
ポスター５

31

プログラム（Program）
P6-4 NSD2/MMSET 発現は形質芽細胞腫瘍の鑑別に有用か？
Is NSD2/MMSET expression useful for the diagnosis of the plasmablastic neoplasms?

藤浪

浅尾
飯田
1

1
春菜
（Haruna Fujinami）
、
木下

優 、成田

朋子 、正木1

1

真介 1

史緒里 1、大島

彩子 、伊藤2

旭 、李1

佳子 1、菊池隆希 1、鈴木政樹 、楠本1

茂 、小松1

智貴 1、戸谷

弘和 、稲垣
1

治仁 1、
宏 2、

名古屋市立大学 医学部 血液・腫瘍内科、2 名古屋市立大学 医学部 臨床病理学

P6-5 t(11;14) 陽性多発性骨髄腫患者の臨床的病理学的な特徴
Clinicopathological analysis of multiple myeloma carrying t(11;14)

安藤

1
知恵
（Tomoe Ando）
、小林

成田

1

健太郎 2、北舘明宏 2、竹内宏紀 2、名塚

正美 2、末永

隆 1、村田翼 1、安部

孝生 2

佳亮 2、三浦大典 2、2

亀田総合病院 臨床検査部、 亀田総合病院 血液腫瘍内科

ポスター 7
5月11日㈯

17:10 - 18:30

ポスター会場多発性骨髄腫の症例報告(治療１）
Case reports (1): treatment in multiple myeloma
座長：佐々木純（Makoto Sasaki）（順天堂大学 医学部 血液学講座）

P7-1 多発性骨髄腫に対する Daratumumab 療法と大腸癌に対する FOLFOX/FOLFIRI 療法を安全に併行しえた一例

A case successfully treated with concurrent chemotherapy of daratumumab for
multiple myeloma and bevacizumab-FOLFOX/FOLFIRI therapy for colon cancer

吉田

粥川
1

1
嵩
（Takashi Yoshida）、古田

竜一 1、鈴木哲1

奈々 1,2、平出賢太郎 1、片岡孝江 1、伊奈

研次 1、名古屋記念病院 血液・化学療法内科、2 名古屋市立大学大学院医学研究科 血液・腫瘍内科学分野

P7-2 自家移植が困難である再発難治性 MM に対する Tandem での血縁者 HLA 一致同種移植実施の効果と安全性に対する考察

Tandem allogeneic stem cell transplantation from an HLA matched sibling donor for
relapsed/refractory multiple myeloma

山田
齊藤

晃子
（Akiko Yamada）
、赤羽

大屋敷

優、片桐
一馬

誠一朗、浅野

大悟、藤本

倫代、勝呂

博昭、伊藤

良和、後藤

多光子、吉澤守孝、大月成一郎、田中

俊輔、森山

裕子、古屋

充、

奈穂子、

東京医科大学病院 血液内科

P7-3 IRd（ixazomib, lenalidomide and dexamethasone）療法開始後早期に腫瘍崩壊症候群を起こした再発難治性骨髄腫

Tumor lysis syndrome (TLS) caused by IRd regimen in a patient with relapsed/refractory multiple myeloma

伊藤
松田

俊輔
（Shunsuke Ito）
、宇賀田
真一朗、岡田

隆宏、池尻

文良、高橋

島根大学医学部附属病院 腫瘍・血液内科

32

典美、島崎

裕正、岡田

勉、三宅

祐介、高橋

隆明、鈴木

史匡、藤本

律朗、鈴宮

淳司

亜弓、

プログラム（Program）

Three myeloma patients complicated by calfilzomib-related hemolysis or TMA

工藤

三輪

哲義

幸治 1、奥田1,2

優子 1、平井理泉 1、谷村

聡 1、竹下昌孝 1,2、

東京北医療センター 血液内科、2 国際骨髄腫先端治療研究センター

ポスター７

1

1
大輔
（Daisuke Kudo）、岡崎

P7-5 IgD λ骨髄腫の治療経験
Experience of IgD λ myeloma treatment

入田博史（Hirofumi Irita）
、藤野
安庸、加藤

元浩、名取

春香、長瀬

一彦

大輔、三井

ゆりか、廣田

愛、恩田

直輝、
ポスター８

倉石

東邦大学医療センター大森病院 血液・腫瘍科

ポスター 8
5月11日㈯

17:10 - 18:30

ポスター会場多発性骨髄腫の症例報告(治療2）
Case reports (2): treatment in multiple myeloma
座長：八木秀男（Hideo Yagi）（奈良総合医療センター 血液腫瘍内科）

P8-1 ダラツムマブと少量のレナリドミドの併用療法が奏功した治療抵抗性 IgD- λ型多発性骨髄腫の一例

A case of IgD- λ relapse/refractory multiple myeloma in which combination therapy
with daratumumab and low-dose lenalidomide was effective

内原潤之介（Jun-nosuke Uchihara）、新垣均

那覇市立病院 血液内科

P8-2 多発性骨髄腫に対する自家末梢血幹細胞移植において TMA を発症した一例
One clinical case of thrombotic microangiopathy developing after engraftment of auto
stem cell transplantation in multiple myeloma

奥田
三輪

優子
（Yuko Okuda）
、谷村
哲義

聡、岡崎

幸治、平井

理泉、工藤

大輔、竹下

昌孝、

東京北医療センター 血液内科

P8-3 新規プロテアソーム阻害剤（Carfilzomib, Ixazomib) を投与した後再発した難治性骨髄腫に対して Daratumumab を使用した 4 症例

Efficacies of daratumumab in four patients with relapsed and refractory multiple
myeloma against new proteasome inhibitors (Carfilzomib, Ixazomib)

池田

加藤
1

1
博
（Hiroshi Ikeda）、高田

淳二 2、小船

雅義 1

ポスター６

㊝ P7-4 Carfilzomib で溶血 /TMA に至った多発性骨髄腫の 3 例

弘一 1,2、村瀬和幸 2、後藤亜香利 1、菊池尚平 1,2、井山

諭 1、

札幌医科大学医学部 血液内科、2 札幌医科大学医学部 腫瘍内科

33

プログラム（Program）
P8-4 再発難治性多発性骨髄腫に対してダラツムマブ併用 Ld 療法（DaraLd）で VGPR を達成
し自家末梢幹細胞移植（ASCT）を施行できた一例

Successful salvage treatment using daratumumab combined with lenalidomide anddexamethasone in a patient with refractory multiple myeloma

王
1

1
梓任
（Ziren Wang）、丸茂

義晃 1、森芙美子 1、楠本

茂 2、飯田真介 2、稲垣淳1

名古屋市立西部医療センター 血液腫瘍内科、2 名古屋市立大学大学院医学研究科 血液・腫瘍内科学

P8-5 Daratumumab 併用化学療法後に B 型肝炎ウイルス再活性化を認めた多発性骨髄腫の 1 例
Hepatitis B virus (HBV) reactivation in a myeloma patient with resolved HBV infection
who received daratumumab containing chemotherapy

菊池

戸谷

飯田
1

1
隆希
（Takaki Kikuchi）、楠本

治仁 、木下史緒理 、浅尾

1

1

真介 1

茂 1、田中優 、成田
1

靖人 2、大島

朋子 、伊藤1

佳子 1、藤浪

旭 、李1

春菜 1、鈴木

政樹 、小松
1

智貴 1、

弘和 1、

名古屋市立大学大学院医学研究科 血液・腫瘍内科学、2 名古屋市立大学大学院医学研究科 病態医科学

ポスター 9
5月11日㈯

17:10 - 18:30

ポスター会場

骨髄腫類縁疾患の症例報告・新規治療法
Case reports: treatment with novel therapy in myeloma-related disorders
座長：堺田惠美子（Emiko Sakaida）（千葉大学医学部附属病院 血液内科）

P9-1 骨生検と MYD88 変異解析で多発性骨髄腫と鑑別し得たリンパ形質細胞性リンパ腫の一例
Bone biopsy and MYD88 mutation analysis is useful for the diagnosis oflymphoplasmacytic lymphoma with lytic bone lesions mimicking multiple myeloma

丸茂
1

1
義晃
（Yoshiaki Marumo）、森

芙美子 1、楠本

茂 2、飯田真介 2、稲垣淳12

名古屋市立西部医療センター 血液・腫瘍内科、 名古屋市立大学大学院医学研究科 血液・腫瘍内科学

P9-2 IgG κ型リンパ形質細胞性リンパ腫に合併した軽鎖沈着症の一例
Light chain deposition disease associated with IgG- κ type lymphoplasmacytic
lymphoma成田健太郎（Kentaro Narita）
、小林

竹内

正美、末永

孝生

宏紀、北舘

明宏、安部

佳亮、三浦

大輔、津島

隆史、

亀田総合病院 血液腫瘍内科

P9-3 アミオダロンと ICD により再発する pulseless VT 後も長期生存を得た全身性 AL アミロ
イドーシスの 1 例

Long-term survival of an AL amyloidosis patient with recurrent pulseless VT treatedwith amiodarone and implantable cardioverter defibrillator (ICD)

入内島

村上
1

34

1
裕乃
（Hirono Iriuchishima）、石埼

博和 3、半田寛1

卓馬 1、吉田くに子 2、飯塚

貴士 2、田村群馬大学医学部 血液内科、2 群馬大学医学部 循環器内科、3 群馬大学医学部保健学科 応用検査学

峻太郎 2、

プログラム（Program）
P9-4 心 AL アミロイドーシスに対するボルテゾミブ療法中に、洞停止や消化管出血などを発症した一例

Cardiac AL amyloidosis that developed sinus arrest and gastrointestinal bleeding
during Bortezomib +Dexamethasone (BD) therapy

寺川

下山
1

1
拓弥
（Takuya Terakawa）、井上

寿 2、荻山秀治 3、筒井

秀作 3

愛 1、高橋雅文 1、石田尚子 1、徳嶺進洋 1、嶋本

新作 2、2

市立伊丹病院 血液内科、 市立伊丹病院 循環器内科、3 市立伊丹病院 消化器内科

Raymond L. Comenzo1、Arnaud Jaccard2、Efstathios Kastritis3、Mathew Maurer4、Jeffrey Zonder5、Monique C. Minnema6、Stefan Schӧnland7、Ashutosh Wechalekar8、Xiang Qin9、Sandra Y. Vasey9、Imran Khan10、Jordan M. Schecter10、鈴木
Giampaolo Merlini12

11
晶子（Akiko Suzuki）
、辻村

亮 11、

Division of Hematology/Oncology, John C. Davis Myeloma and Amyloid Program, Tufts Medical Center, Boston,

MA、2CHU Dupuytren, Limoges, France、3Univ. of Athens School of Medicine, Alexandra General Hospital,
Athens, Greece、4Presbyterian Hospital and Vanderbilt Clinic, New York, NY、5Barbara Ann Karmanos Cancer
Institute, Detroit, MI、6UMC Utrecht, Utrecht, Netherlands、7Heidelberg Univ. Hospital, Heidelberg, Germany、
8

ポスター９

1

ポスター８

P9-5 Phase 3 Study of Cyclophosphamide/Bortezomib/Dexamethasone (CyBorD) ±Daratumumab (DARA) in Newly Diagnosed Amyloid Light Chain Amyloidosis: ANDROMEDA

Univ. College London and the Royal Free London NHS Foundation Trust, London, UK、9Janssen Research &ポスター

Development, LLC, Spring House, PA, USA、10Janssen Research & Development, LLC, Raritan, NJ, USA、
11

Janssen Pharmaceutical K.K., Tokyo, Japan、12Scientific Institute Policlinico San Matteo, University of Pavia,

Italy

10

ポスター 10
5月11日㈯

17:10 - 18:30

ポスター会場

移植適応多発性骨髄腫の治療1
Stem-cell transplant in multiple myeloma (1)
座長：角南

P10-1

一貴（Kazutaka Sunami）（国立病院機構 岡山医療センター 血液内科）

多発性骨髄腫患者に対する自家移植後の地固め療法のリスクとベネフィット
Risks and benefits of consolidation therapy after autologous stem cell transplantation
for multiple myeloma

依田
高羽

在理
（Akari Yoda）
、永田
理光、安達

泰之、伊東

美和、竹村

兼成、小野

侑治郎、高木孝明

文智、中野洸太郎、内山哲、坂本奈美、

浜松医科大学医学部附属病院 血液内科

P10-2

移植適応多発性骨髄腫において初回自家末梢血幹細胞採取不良が予後に与える影響
The impact of poor PBSC mobilization on the outcome of patients with multiple
myeloma長井

1
友莉恵（Yurie Nagai）
、三村

原

5

三川

紫緒 1,2、塚本暁 、趙祥吉 1、竹田竜桓 、中世古6

尚也 1,2、石井勇輔 1、武内

知昭

、堺田

1,7

改 1、一色正博 1、大和田惠美子1

佑介 1、杉田千桂子 1、井関泰雅 3、大島徹 1,2、深澤

渚 1、

元晴 4、

1

2

千葉大学医学部附属病院 血液内科、 千葉大学医学部附属病院 輸血・細胞療法部、3 国保大網病院 血液内科、

4

JCHO 船橋中央病院 内科、5 千葉ろうさい病院 腫瘍血液内科、6 千葉県済生会習志野病院 血液内科、

7

国際医療福祉大学医学部 血液内科

35

プログラム（Program）
P10-3

当院で行った再発・難治多発性骨髄腫に対する非血縁者間骨髄移植 14 例の検討
Unrelated bone marrow transplantation for relapsed/refractory multiple myeloma

塚田信弘（Nobuhiro Tsukada）、梨本

吉識

由実子、阿部有、石田淳一郎、宇藤

禎夫、鈴木

唯、佐藤

憲史

広太、宮崎

寛至、小倉

瑞生、

日本赤十字社医療センター 血液内科

P10-4

移植適応の初発多発性骨髄腫に対する modified RVD-lite の有効性と安全性に関する後方視的解析

Retrospective analysis of the efficacy and safety of modified bortezomib-lenalidomidedexamethasone litefor transplant eligible NDMM

岡塚貴世志
（Kiyoshi Okazuka）
、石田

宮崎

寛至、小倉

瑞生、吉識

禎夫、余語

由実子、阿部

孝夫、梨本

有、塚田

淳一郎、宇藤

信弘、鈴木

憲史

唯、佐藤

広太、

日本赤十字社医療センター 血液内科

P10-5

メルファランを前処置とした自家造血幹細胞移植症例における食事調整による経口摂取と早期経静脈栄養の比較

Early Parental Nutrition Versus Food Modification in Patients Undergoing Autologous
Transplantation

宮崎

寛至（Kanji Miyazaki）
、石田

禎夫、鈴木

憲史

日本赤十字社医療センター 血液内科

ポスター 11
5月12日㈰14:30 - 15:50

ポスター会場

移植適応多発性骨髄腫の治療2Stem-cell transplant in multiple myeloma (2)
座長：塚田

P11-1

信弘（Nobuhiro Tsukada）（日本赤十字医療センター 血液内科）

自家移植適応の初発高リスク多発性骨髄腫に対するカルフィルゾミブ・レナリドミド・
デキサメサゾンによる寛解導入療法

Carfilzomib with lenalidomide and dexamethasone prior to high-dose therapy for
newly diagnosed high-risk multiple myeloma

小山大輔（Daisuke Koyama）
、伊藤

理恵、山本

里美、井本

直人、倉橋

信悟、杉浦

勇

豊橋市民病院 血液・腫瘍内科

P11-2

当院における多発性骨髄腫に対する強度減弱前処置による同種造血幹細胞移植の後方視的解析

Retrospective analysis of reduced intensity conditioning allogeneic hematopoietic
transplantation for multiple myeloma at Chiba university hospital

武内

長井

日野

1
正博
（Masahiro Takeuchi）、田波

友莉恵 、三科1

裕太郎 1、
塚本

中世古
1

祥吉 1、
三川

知昭 1,3、堺田

惠美子 1

貴彬 1、畑中

美貴 、一色1

紫緒 1,2、竹田康人 1、柴宮

佑介 、栢森1

勇輔 1、三村明日香 1、石井健介 、木村1

尚也 1,2、大和田

改 1、

賢司 、高石1

千桂子 1、井関浩司 1、
徹 1,2、

千葉大学医学部附属病院 血液内科、2 千葉大学医学部附属病院 輸血・細胞療法部、3 国際医療福祉大学医学部

血液内科

36

達三 、山﨑1

プログラム（Program）
P11-3 CyBorD 寛解導入療法を用いた初発多発性骨髄腫に対する自己末梢血幹細胞移植の長期成績
Long-term outcome of CyBorD induction and autologous peripheral blood stem celltransplantation for patients with newly diagnosed multiple myeloma

倉橋

杉浦
1

P11-4

1
信悟
（Shingo Kurahashi）、奥野

真吾 1,2、伊藤勇1

理恵 1、山本里美 1、小山大輔 1、井本直人 1、

豊橋市民病院 血液・腫瘍内科、2 名古屋大学大学院医学系研究科 血液・腫瘍内科学

移植適応多発性骨髄腫患者に対する６サイクルの寛解導入療法（VRd/KRd）の安全性と有効性の検討Feasibility of 6 cycles of VRd/KRd as an induction therapy prior to stem-cell collection
in transplant-eligible multiple myeloma

吉原享子（Kyoko Yoshihara）
、吉原

哲、玉置

広哉、岡田

昌也、藤盛

好啓

兵庫医科大学病院 血液内科

ポスター 12
5月12日㈰14:30 - 15:50

ポスター会場多発性骨髄腫の病態と疫学研究
座長：和泉

P12-1

ポスター

Pathogenesis and epidemiology of multiple myeloma
透（Tohru Izumi）（栃木県立がんセンター 血液内科）

10

日本における多発性骨髄腫への新規薬剤導入の影響：罹患率と死亡率の経年変化の評価

碓井

松尾
1

1,4
喜明
（Yoshiaki Usui）、
伊藤

秀美 1、小栁恵太郎 5

友理子 1、松田

智大 2、片野田耕太 3、前田

嘉信 4、

11

愛知県がんセンター研究所 がん予防医療研究領域 がん情報・対策研究分野、2 国立がん研究センター
ポスター

がん情報対策センター がん登録センター、3 国立がん研究センター がん情報対策センター
がん統計・総合解析研究部、4 岡山大学大学院 医歯薬総合研究科 血液・腫瘍・呼吸器内科学、
5

P12-2

愛知県がんセンター研究所 がん予防医療研究領域 がん予防研究分野

12

日常診療における多発性骨髄腫の治療成績とそれに及ぼす予後因子の検討
Real-world patient characteristics and outcomes of multiple myeloma

秋月

1
渓一
（Keiichi Akizuki）
、松岡

亀田

拓郎 、幣

前田

P12-3

ポスター

The impact of novel agents on multiple myeloma: trend of incidence and mortality inJapan

宏一 6、佐藤1

誠一 7、河野光太郎 、日髙1

均 2、外山孝典 3、石崎淳三 4、山下

智徳 、久冨木庸子 、下田和哉

浩 2、武内1

正紀 2、関根1

雅明 1、上運天
1

清 5、河野綾子 1、田平

徳明 5、

優貴 1、

1

宮崎大学医学部付属病院 内科学講座消化器血液学分野、2 古賀総合病院、3 宮崎県立延岡病院、4 愛泉会日南病院、

5

宮崎県立宮崎病院、6 国立病院機構 都城医療センター、7 医療法人啓仁会 城南病院

多発性骨髄腫における長期生存症例の臨床的特徴
Long-term multiple myeloma survivors; clinical features of patients who survived
longer than 10-years

寺尾
成田

俊紀
（Toshiki Terao）、北館
健太郎、竹内

正美、末永

明宏、安部

孝生

佳亮、津島

隆史、小林

宏紀、三浦

大典、

亀田総合病院

37

プログラム（Program）㊝ P12-4 多発性骨髄腫患者における PIM2, TAK1 の重要性

PIM2 and phosphorylated TAK1 expression as important prognostic factors in patientswith multiple myeloma

中村

小田

原田

P12-5

1
信元
（Shingen Nakamura）、三木

浩和 2、寺町

武志 、藤井1

明日香 1、岡本恵暢 1、大浦

志朗 、賀川1

1

雅博 1、曽我部久美子 、安倍順平 3、天真

公子 1、高橋正博

寬文 4、日浅真美子 1、岩佐1

雅博 5、

昌美 1、宇高憲吾 1、1

徳島大学大学院医歯薬学研究部血液・内分泌代謝内科学、2 徳島大学病院輸血・細胞治療部、

3

徳島大学大学院医歯薬学研究部口腔組織学分野、4 徳島大学大学院医歯薬学研究部口腔顎顔面矯正学、

5

徳島大学大学院医歯薬学研究部生体材料工学分野

SMM の後方視的検討：High risk SMM の抽出と早期治療の是非
Retrospective study of SMM : extraction of high risk SMM and early treatment

麻奥

勝谷

1

1
英毅
（Hideki Asaoku）、板垣

慎也 、岩戸康治

22

充弘 1、片山雄太 1、岡谷健史 1、今中亮太 1、許鴻平 1、

広島赤十字・原爆病院 血液内科、2 広島赤十字・原爆病院 検査部

ポスター 13
5月12日㈰14:30 - 15:50

ポスター会場

治療法の研究（抗体療法）
Monoclonal antibodies in multiple myeloma
座長：林敏昭（Toshiaki Hayashi）（手稲渓仁会病院 北海道骨髄腫センター）

P13-1

当科での Daratumumab 5 例の使用経験
Experience with the Use of Daratumumab in Five Patients at Our Department

関口

坂尻

野口

P13-2

1
康宣
（Yasunobu Sekiguchi）、飯塚

さくら 1、冨田雅章

茂樹 2、泉1

弘子 1、瀧澤浩 2、大久保春子 1、若林

光夫 3、中村

睦 1、杉元

紀子 4、澤田

啓二 1、

朝寛 4、小松1

順天堂大学医学部附属浦安病院 血液内科、2 順天堂大学医学部附属浦安病院 病理部、

3

順天堂大学医学部附属浦安病院 輸血学研究室、4 順天堂大学医学部附属浦安病院 臨床検査医学科、

5

順天堂大学医学部附属順天堂医院 血液内科

当科での Elotuzumab 9 例の使用経験
Experience with the Use of Elotuzumab in Nine Patients at Our Department

瀧澤

冨田

P13-3

1
春子
（Haruko Takizawa）
、関口

茂樹 、泉
2

浩 、大久保2

康宣 1、飯塚光夫 、中村3

弘子 1、若林紀子 、澤田4

睦 1、杉元朝寛 、小松4

啓二 1、坂尻

則夫 、野口51

順天堂大学医学部附属浦安病院 血液内科、2 順天堂大学医学部附属浦安病院 病理部、

3

順天堂大学医学部附属浦安病院 輸血学研究室、4 順天堂大学医学部附属浦安病院 臨床検査医学科、

5

順天堂大学医学部附属順天堂医院 血液内科

さくら 1、雅章 1

実臨床におけるダラツムマブの安全性と有効性についての検討
The safety and efficacy of daratumumab in a real world data

津島
北館

隆史
（Takafumi Tsushima）
、小林
明宏、竹内

正美、末永

亀田総合病院 血液腫瘍内科

38

則夫 5、

孝生

宏紀、寺尾

俊紀、安部

佳亮、三浦

大典、成田

健太郎、

プログラム（Program）
P13-4

Updated Analysis of Daratumumab Plus Rd in East Asian and Japanese Relapsed/
Refractory Multiple Myeloma (RRMM) Patients: POLLUX

竹迫

松本

鈴木
1

1
直樹
（Naoki Takezako）、Meletios A Dimopoulos2、飯田

守生 6、小杉憲史

真介 3、岡本真一郎 4、品川篤司 5、

浩史 7、Sung-Soo Yoon8、Shang-Yi Huang9、Xiang Qin10、Ming Qi10、11

独立行政法人国立病院機構 災害医療センター 血液内科、2National and Kapodistrian University of Athens,

Athens, Greece、3 名古屋市立大学大学院医学研究科 血液・腫瘍内科学、4 慶應義塾大学病院 血液内科、
5

日立総合病院 血液・腫瘍内科、6 国立病院機構 渋川医療センター 血液内科、7 大垣市民病院 血液内科、8Seoul

National University Hospital, Seoul, Korea、9National Taiwan University Hospital, Taipei, Taiwan、10Janssen
Research & Development, LLC, Spring House, PA, USA、11 日本赤十字社医療センター 血液内科

P13-5

ELd 療法の長期効果が期待できる患者の解析
Analysis of patients who can expect long-term effects of ELd therapy

松本

澤村
1

P13-6

1
守生
（Morio Matsumoto）、田原

研一 1、三原

守夫 2

正大 1、明石直樹 1、磯田

淳 1、

国立病院機構渋川医療センター 血液内科、2 国立病院機構渋川医療センター 臨床研究部

実臨床における再発・難治性骨髄腫患者に対する ERd 療法の効果
Efficacy of elotuzumab plus lenalidomide/dexamethasone in patients with relapsed/refractory multiple myeloma in the real-world practice setting

添田

田中

1

1
沙織
（Saori Soeda）、山下

淳司 5、佐々木純 6、小松卓也 1、磯田則夫 6、安井

淳 2、鈴木寛 7、今井2

一史 3、木口陽一 7、石橋

亨 4、田中紀奈 5、真理子 8、田村秀人 93

聖路加国際病院 血液内科、 国立病院機構渋川医療センター 血液内科、 東京慈恵会医科大学附属柏病院

腫瘍・血液内科、4 中国中央病院 血液内科、5 東京女子医科大学 血液内科、6 順天堂大学医学部順天堂医院 血液内科、
7

東京大学医科学研究所 血液腫瘍内科、8 日本医科大学微生物学・免疫学、9 日本医科大学血液内科 血液内科

ポスター 14
5月12日㈰14:30 - 15:50

ポスター会場ポスター

治療法の研究（プロテアソーム阻害薬）
Proteasome inhibitors in multiple myeloma
隆之（Takayuki Ishikawa）（神戸市立医療センター 中央市民病院 免疫・血液内科）

P14-1

血清 ICTP が高値を示す形質細胞腫瘍患者におけるボルテゾミブ投与の有効性

12

ポスター

座長：石川

Bortezomib overcomes poor prognosis conferred by high serum C-terminal
telopeptide of type I collagen in patients with untreated plasma cell disorder大山悠（Yu Oyama）
、本田

晃、遠山

和博、黒川

13

峰夫

P14-2

再発又は難治性の多発性骨髄腫に対するニンラーロ ® カプセル使用成績調査における早期中止例の中間解析

14

The interim analysis of post-marketing surveillance of ixazomib for relapsed/refractory
multiple myeloma, focusing on early discontinued cases

柿本
1

1
宜秀
（Yoshihide Kakimoto）
、星野

ポスター

東京大学医学部附属病院 血液・腫瘍内科

京2

武田薬品工業株式会社 日本オンコロジー事業部メディカルアフェアーズ部、2 武田薬品工業株式会社

ジャパンファーマビジネスユニットメディカルアフェアーズ部

39

プログラム（Program）
P14-3

当院における再発・難治性多発性骨髄腫に対する Carfilzomib の治療成績
Outcome of treatment of relapsed / refractory multiple myeloma with Carfilzomib

守山
角南

喬史
（Takashi Moriyama）
、村上

裕之、福見

一貴

拓也、石川

立則、吉岡

尚徳、牧田

雅典、

国立病院機構岡山医療センター 血液内科

P14-4 当施設における多発性骨髄腫に対するカルフィルゾミブ併用療法の有効性と安全性の検討
Efficacy and safety of carfilzomib containing regimens for multiple myeloma in our
institution

木口
瀨﨑

亨
（Toru Kiguchi）
、野村
伸夫

奈穂、岡本

幸代、黒井

大雅、谷

勝真、遠西

大輔、

中国中央病院 血液内科

P14-5

Phase 2 Trial of Pomalidomide + Low-Dose Dexamethasone + Daratumumab in
Relapsed Refractory Multiple Myeloma: Safety, Efficacy, and Immune Profile

David S. Siegel1、Gary J Schiller2、Christy Samaras3、Jesus Berdeja4、Siddhartha Ganguly5、Jeffrey Matous6、Kevin Song7、Christopher S. Seet8、Giampaolo Talamo9、Mirelis Acosta-Rivera10、Michael Bar11、Donald Quick12、Bertrand Anz13、Gustavo Fonseca14、Donna Reece15、Amit Agarwal16、Weiyuan Chung16、William Pierceall16、Faiza Zafar16、Nizar J. Bahlis17
1

John Theurer Cancer Center, Hackensack University Medical Center, Hackensack, NJ, United States、2David

Geffen School of Medicine at University of California, Los Angeles, CA, United States、3Cleveland Clinic,
Cleveland, OH, United States、4Sarah Cannon Research Institute, Nashville, TN, United States、5The Universityof Kansas Cancer Center, Fairway, KS, United States、6Colorado Blood Cancer Institute, Denver, CO, UnitedStates、7Vancouver General Hospital, Vancouver, BC, Canada、8University of California, Los Angeles Medical
Center, Los Angeles, CA, United States、9Penn State Hershey Cancer Institute, Hershey, PA, United States、
10

Fundación de Investigación, San Juan, Puerto Rico、11Stamford Hospital, Stamford, CT、12Joe Arrington

Cancer Research and Treatment Center, Lubbock, TX, United States、13Tennessee Oncology, Chattanooga, TN,
United States、14Florida Cancer Specialists, St Petersburg, FL, United States、15Princess Margaret Cancer
Centre, Toronto, ON, Canada、16Celgene Corporation, Summit, NJ, United States、17University of Calgary,
Calgary, AB, Canada

ポスター 15
5月12日㈰14:30 - 15:50

ポスター会場

治療法の研究（レナリドミド・その他）
Lenalidomide and other treatment modality in multiple myeloma
座長：三木

P15-1

浩和（Hirokazu Miki）（徳島大学病院 血液内科）

再発又は難治性多発性骨髄腫に対する段階的増量レナリドミド療法による治療戦略
Therapeutic strategy with dose-escalating lenalidomide for relapsed or refractory
multiple myeloma

北川

兼村
1

40

1
順一
（Junichi Kitagawa）、金田

信宏 1、笠原千嗣 2、清水2

裕人 1、山口雅仁 1、原公大 1、松本

武志 4、澤田3

拓郎 1、中村

道夫 3、鶴見寿44

博 1、二宮空暢 1、

岐阜大学医学部 血液内科、 岐阜市民病院 血液内科、 岐阜赤十字病院 血液内科、 松波総合病院 血液内科

プログラム（Program）
高齢未治療多発性骨髄腫における Ld 療法前後の免疫プロファイルの変化と無増悪期間と

ポスター

P15-2

Correlation between immune profile changes and time to progression in patients with
newly diagnosed multiple myeloma treated with Ld therapy

16の関連の検討

小林
1

P15-3

1
敬宏
（Takahiro Kobayashi）、藤岡

優樹 1,2、池田

翔 1、西川博嘉 2、髙橋

直人 1

秋田大学大学院医学系研究科 血液内科、2 国立がん研究センター 免疫 TR 分野

レナリドミド治療前後における CRBN 関連遺伝子の発現量変化と遺伝子変異の解析
Analysis of expression levels and mutations in CRBN related genes at pre- and postlenalidomide treatment in multiple myeloma

木下
戸谷

史緒理
（Shiori Kinoshita）
、李
治仁、成田

朋子、伊藤

政樹、立田

旭、楠本

卓登、浅野

茂、小松

有彩、青木

弘和、飯田

奨、金森

真介

貴之、

名古屋市立大学病院 血液・腫瘍内科

P15-4

ボルテゾミブとレナリドミドに不応となった多発性骨髄腫症例の予後研究
Survival of Patients with Multiple Myeloma That Is Refractory to Both Bortezomib andLenalidomide: A Retrospective Study

宮崎寛至（Kanji Miyazaki）
、石田

禎夫、鈴木

憲史

日本赤十字社医療センター 血液内科

P15-5

移植後微小残存病変に対するエロツズマブ併用体外増幅ＮＫ細胞輸注療法第一例目の報告Ex-vivo expanded NK cell therapy combined with Elotuzumab for MRD after
autologous stem cell transplantation - A report of the first case -

萩原

町島
1

1
將太郎
（Shotaro Hagiwara）、王

智人 3、石山

みどり 1、吉永

艶華 1、小林健太郎 1、志関博人 2、加藤雅幸 1、菅野豊 1、飯塚仁 2、田中有希 1、田中
淳司 1

紀奈 1、

2

東京女子医科大学医学部 血液内科学講座、 東京女子医科大学医学部 輸血・細胞治療部、3 済生会栗橋病院

血液内科

ポスター 16
5月12日㈰14:30 - 15:50

ポスター会場

治療法の研究（ポマリドミド）
Pomalidomide in multiple myeloma
座長：杉浦

P16-1

勇（Isamu Sugiura）（豊橋市民病院 血液・腫瘍内科）

ポマリドミド＋低用量デキサメタゾン（Pd）療法の有効性と安全性

ポスター～当院の再発難治性多発性骨髄腫（RRMM）26 例の後方視的解析～
Efficacy and safety of pomalidomide and low dose dexamethasone ; retrospective
analysis of 26 relapse and refractory multiple myeloma in our hospital

明石
1

1
直樹
（Naoki Akashi）、三原

正大 1、田原研一 1、磯田淳 1、松本守生 1、澤村14

守夫 2

渋川医療センター 血液内科、2 渋川医療センター 臨床研究部
ポスター
15

41

プログラム（Program）
P16-2

当科での Pomalidomide 16 例の使用経験
Experience with the Use of Pomalidomide in Sixteen Patients at Our Department

若林

坂尻

野口

P16-3

1
睦
（Mutsumi Wakabayashi）、関口

さくら 、冨田
1

雅章 1

茂樹 、泉
2

康宣 1、飯塚浩 、大久保2

弘子 1、瀧澤

光夫 、中村3

春子 1、杉元

紀子 、澤田4

啓二 1、

朝寛 、小松41

順天堂大学医学部附属浦安病院 血液内科、2 順天堂大学医学部附属浦安病院 病理部、

3

順天堂大学医学部附属浦安病院 輸血学研究室、4 順天堂大学医学部附属浦安病院 臨床検査医学科、

5

順天堂大学医学部附属順天堂医院 血液内科

則夫 5、当院における形質細胞腫を伴う多発性骨髄腫に対する、ポマリドミド・シクロホスファ
ミド・デキサメタゾン併用療法の使用成績

Pomalidomide, cyclophosphamide, and dexamethasone as an efficient regimen for
extramedullary multiple myeloma

井手史朗（Shiro Ide）
、大原

慎、内田

智之、井上

盛浩、華

見、萩原

政夫

永寿総合病院 血液内科

P16-4

当院におけるポマリドマイド / デキサメタゾン療法 34 例の後方視的検討
Retrospective analysis of pomalidomide with dexametasone for 34 patients withrelapsed/refractory multiple myeloma; A single center experience

淵田

島崎

1
真一
（Shin-ichi Fuchida）
、角

千尋 1

陽子 2、民西葉子 1、松井紗央梨 1、初瀬

真弓 1、村頭

智 1、

1

JCHO 京都鞍馬口医療センター 血液内科、2JCHO 京都鞍馬口医療センター 薬剤科

P16-5

ボルテゾミブおよびレナリドミドレジメン抵抗性多発性骨髄腫に対する PomCyDex 療法
PomCyDex therapy for double-refractory multiple myeloma

矢野寛樹（Hiroki Yano）、中村

JA 愛知厚生連海南病院 血液内科

42

智幸、中島

貴裕

プログラム（Program）

5月12日㈰14:30 - 15:50

ポスター

ポスター 17
ポスター会場

16

レジストリー研究と新規治療法の開発
座長：河野

P17-1

ポスター

Registry data and novel therapy in multiple myeloma
和（Yawara Kawano）（熊本大学病院 血液・膠原病・感染症内科）

17

Development of a Predictive Model of Multiple Myeloma Patient Outcomes Based on
Treatment Sequencing Using the Connect® MM Patient Registry

Sundar Jagannath1、Robert M. Rifkin2、Cristina J. Gasparetto3、Kathleen Toomey4、Brian G.M. Durie5、James W. Hardin6、Howard Terebelo7、Lynne Wagner8、Mohit Narang9、Shankar Srinivasan10、Lihua Yue10、Amani Kitali10、Gail Larkins10、Amit Agarwal10、

Rafat Abonour11
1

Mount Sinai Hospital, New York, NY、2US Oncology Research, Rocky Mountain Cancer Centers, Denver, CO、

3

Duke University Medical Center, Durham, NC、4Steeplechase Cancer Center, Somerville, NJ、5Cedars-Sinai

Samuel Oschin Cancer Center, Los Angeles, CA、6University of South Carolina, Columbia, SC、7Providence
Cancer Institute, Southfield, MI、8Wake Forest School of Medicine, Winston-Salem, NC、9US Oncology
Research, Maryland Oncology Hematology, Columbia, MD、10Celgene Corporation, Summit, NJ、11Indiana
University Simon Cancer Center, Indianapolis, IN

P17-2

Connect® MM Registry: Treatment Choices and Outcomes for Patients with Multiple
Myeloma after Relapse on Lenalidomide Maintenance Therapy

Sundar Jagannath1、Mohit Narang2、Sikander Ailawadhi3、Robert M. Rifkin4、Howard R. Terebelo5、Kathleen Toomey6、Brian G.M. Durie7、James W. Hardin、Cristina J. Gasparetto9、Lynne Wagner10、James Omel11、Shankar Srinivasan12、Amani Kitali12、Amit Agarwal12、Rafat Abonour13
1

Mount Sinai Hospital, New York, NY, USA、2US Oncology Research, Columbia, MD, USA、3Mayo Clinic,

Jacksonville, FL, USA、4Rocky Mountain Cancer Centers US Oncology, Denver, CO, USA、5Providence Cancer
Institute, Novi, MI, USA、6Steeplechase Cancer Center, Somerville, NJ, USA、7Cedars-Sinai Medical Center, Los
Angeles, CA, USA、8University of South Carolina, Columbia, SC, USA、9Duke University Medical Center,
Durham, NC, USA、10Wake Forest School of Medicine, Winston-Salem, NC, USA、11Myeloma Research
Advocate/Advisor Grand Island, NE, USA、12Celgene Corporation, Summit, NJ, USA、13Indiana University,
Indianapolis, IN, USA

43

プログラム（Program）㊝ P17-3 Pomalidomide + Bortezomib + Low-Dose Dexamethasone in Relapsed / Refractory
Multiple Myeloma After 1 Prior Line of Therapy: A Subanalysis of OPTIMISMM

Kosei Matsue1、Meletios Dimopoulos2、Katja Weisel3、Philippe Moreau4、Larry Anderson Jr D.5、Darrell White6、Jesus Miguel San7、Pieter Sonneveld8、Monika Engelhardt9、Matthew Jenner10、

Jan Dürig11、Michel Pavic12、Morten Salomo13、Xin Yu14、Tuong Nguyen Vi14、Tsvetan Biyukov15、Teresa Peluso15、Paul Richardson16
1

Kameda Medical Center, Kamogawa-shi, Chiba, Japan、2National and Kapodistrian University of Athens,

Athens, Greece、3University Hospital of Tuebingen, Tuebingen, Germany、4University Hospital Hôtel-Dieu,
Nantes, France、5University of Texas Southwestern Medical Center, Dallas, TX, United States、6Dalhousie
University and Queen Elizabeth II Health Sciences Centre, Halifax, Canada、7Clinica Universidad de Navarra,
CIMA, IDISNA, Pamplona, Spain、8Erasmus MC Cancer Institute, Rotterdam, the Netherlands、
9

Universitätsklinikum Freiburg, Freiburg, Germany、10Southampton General Hospital, Southampton, United

Kingdom、11University Hospital Essen, Essen, Germany、12Centre Hospitalier Universitaire De Sherbrooke (CHUS)- Centre de Recherche Clinique Etienne-Le Bel (CRCELB) Hopital Fleurimont, Sherbrooke, Canada、
13

Copenhagen University Hospital, Rigshospitalet, Kobenhavn, Denmark、14Celgene Corporation, Summit, NJ,

United States、15Celgene International, Boudry, Switzerland、16Jerome Lipper Multiple Myeloma Center,
Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, UnitedStates

P17-4

RRMM に対するポマリドミド＋ボルテゾミブ＋低用量デキサメタゾン（PVd）併用療法 :OPTIMISMM 試験 日本人サブグループ解析

Pomalidomide + Bortezomib + Low-Dose Dexamethasone (PVd) in Relapsed / Refractory
Multiple Myeloma: OPTIMISMM Japanese Subgroup Analysis
角南

玉越

1
一貴
（Kazutaka Sunami）、末永

孝生 2、鈴木憲史 3、竹迫直樹 4、品川裕巳 6、Biyukov Tsvetan7、Peluso Teresa7、Richardson Paul8

篤司 5、櫻井早苗 6、

1

独立行政法人国立病院機構 岡山医療センター 血液内科、2 医療法人鉄蕉会 亀田総合病院 血液・腫瘍内科 、3

日本赤十字社医療センター 骨髄腫アミロイドーシスセンター、4 独立行政法人国立病院機構 災害医療センター

血液内科 、5 株式会社日立製作所 日立総合病院 血液腫瘍内科、6 セルジーン株式会社、7Celgene International
Sàrl、8Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute

P17-5

Bortezomib/melphalan/prednisone (VMP)±Daratumumab in Transplant-ineligible
Newly Diagnosed Multiple Myeloma: ALCYONE Update with Japanese Subanalysis

藤崎

1
智明
（Tomoaki Fujisaki）、石川隆之 2、高松

Anupa Kudva5、Susan Wroblewski6、Ming Qi6、長藤1

博幸 3、鈴木宏司 7

憲史 4、Jianping Wang5、

2

日本赤十字社 松山赤十字病院 内科、 神戸市立医療センター 中央病院 免疫・血液内科、3 金沢大学

血液・呼吸器内科、4 日本赤十字社医療センター 血液内科、5Janssen Research & Development, LLC、6Janssen
Research and Development, LLC、7 久留米大学医学部 血液・腫瘍内科部門

44プログラム（Program）

ポスター 18
5月12日㈰14:30 - 15:50

ポスター会場多発性骨髄腫の合併症・有害事象対策・診療支援１
座長：若山

P18-1

ポスター

Complications, adverse events, and supportive care in multiple myeloma (1)聡雄（Toshio Wakayama）（島根県立中央病院 検査診断科）

効果と医療経済の観点からみた造血幹細胞動員促進薬 Plerixafor

17

小倉

瑞生
（Mizuki Ogura）
、愛葉

佐藤

広太、宮崎

寛至、吉識

美奈、塚田

由実子、阿部

信弘、梨本

有、岡塚

淳一郎、余語貴世志、石田

孝夫、宇藤

禎夫、鈴木

ポスター

Plerixafor is clinically and economically effective as mobilization protocol for
peripheral blood stem cell apheresis

唯、

憲史

18

日本赤十字社医療センター 血液内科

The Safety profile of daratumumab in Japanese patients with relapsed/refractory
multiple myeloma: post-marketing surveillance of the first 12 weeks

宮田

有田

1
泰彦
（Yasuhiko Miyata）、滝澤

恵梨子 、遠城4

健太郎

1

愛美 1、高岸正幸 2、川合治功 2、藤野明子 3、矢島勉 4、

1

Medical Affairs Division, Janssen Pharma K. K.、2Safety Risk Management Division, Janssen Pharma K. K.、

3

4
Japan Safety & Surveillance Division, Janssen Pharma K. K.、
Quantitative Sciences Division, Janssen Pharma K. K.

P18-3

ダラツムマブ (Dara) 療法で infusion reaction を起こさない当院の取り組みの検討
A study on the approach of Daratumumab (Dara) treatment without infusion reaction
at our institution

板垣充弘（Mitsuhiro Itagaki）
、麻奥

岡谷

健史、今中

亮太、許

英毅、片山

鴻平、勝谷

雄太、寺崎

慎也、牟田

毅、岩戸

達哉、幸地
康治

祐、陳之内

文昭、

広島赤十字・原爆病院 血液内科

P18-4

IRd 療法の服薬アドヒアランス向上のための薬剤師の役割
Role of pharmacists to improve medication adherence of IRd therapy

新行内

松本
1

1
健一
（Kenichi Shingyouuchi）
、栗原

守生 2

りか 1、工藤彰 1、蟻川勝 1、飯合等 1、

渋川医療センター 薬剤部、2 渋川医療センター 血液内科

ポスター 19
5月12日㈰14:30 - 15:50

ポスター会場多発性骨髄腫の合併症・有害事象対策・診療支援２
Complications, adverse events, and supportive care in multiple myeloma (2)
座長：磯田

P19-1

淳（Atsushi Isoda）（国立病院機構 渋川医療センター 血液内科）

未治療多発性骨髄腫患者における updated チャールソン併存疾患指数の意義
Impact of updated Charlson comorbidity index on survival in patients with newly
diagnosed multiple myeloma

稲垣
1

1
淳
（Atsushi Inagaki）、楠本

茂 2、丸茂義晃 1、森芙美子 1、飯田真介 22

名古屋市立西部医療センター 血液 ･ 腫瘍内科、 名古屋市立大学大学院医学研究科 血液 ･ 腫瘍内科学

45

ポスター

P18-2

19

プログラム（Program）
P19-2

IMiDs による皮疹に対するステロイド併用下での漸増再投与法の試み
Desensitization to IMiDs-induced skin rush in a patient with multiple myeloma

大原慎（Shin Ohara）
、井手

史朗、内田

智之、井上

盛浩、華

見、萩原

政夫

永寿総合病院 血液内科

P19-3

Infusion reaction 軽減のためのダラツムマブ初回低速投与
Slow administration of daratumumab for frail myeloma patients

奥田

1
慎也
（Shinya Okuda）、木内

貴章 2、上杉章紀 2、百瀬純子 2、竹林

ちあき 1

1

JR 東京総合病院 血液・腫瘍内科、2JR 東京総合病院 薬剤部

P19-4

患者に対してセンシティブな内容（性交渉や避妊等）を説明する医療従事者向け教育プ
ログラムの策定に関する研究

Development of educational program for the medical practitioners who engage in theinterview to the patients about sensitive contents

鈴木

P19-5

1
憲史
（Kenshi Suzuki）、有田

悦子 2、林昌洋 3、服部

豊 4、西村倫子 5、村上

博和 6

1

2

日本赤十字社医療センター 骨髄腫・アミロイドーシスセンター、 北里大学薬学部医療心理学部門、

3

虎の門病院薬剤部、4 慶應義塾大学薬学研究科、5 がん研究会有明病院血液腫瘍科、

6

群馬大学大学院保健学研究科

治療後に高アミラーゼ血症を呈した多発性骨髄腫症例の検討
Hyperamylasemia developing after treatment for multiple myeloma

中村
掛川

裕一
（Yuichi Nakamura）
、坂本
絵美、内田

優美子、森

朋之、奥田

茂久、別所

正美

糸子、阿久澤

有、伊藤

善啓、脇本

直樹、

埼玉医科大学病院 血液内科

ランチョンセミナー 1
5月11日㈯座長：柴山LS1

12:00 - 12:50

第1会場

浩彦（Hirohiko Shibayama）（大阪大学大学院 医学系研究科 血液・腫瘍内科）

Real-World Evidence and Clinical Implications

Sundar Jagannath

Mount Sinai Hospital, New York, NY, USA〈共催：セルジーン株式会社〉

ランチョンセミナー 2
5月11日㈯座長：鈴木LS2

12:00 - 12:50

第2会場

憲史（Kenshi Suzuki）（日本赤十字社医療センター 骨髄腫アミロイドーシスセンター）

新薬時代における progression-free plateau
Progression-free plateau in era of new agents

太田健介（Kensuke Ohta）

LIGARE 血液内科太田クリニック・心斎橋〈共催：ブリストル・マイヤーズ スクイブ株式会社〉

46

プログラム（Program）

ランチョンセミナー 3
5月12日㈰座長：竹迫

LS3

12:10 - 13:00

第1会場

直樹（Naoki Takezako）（国立病院機構災害医療センター）

Unmet medical needs in maintenance treatment for newly diagnosed multiple
myeloma (NDMM)

Wee Joo Chng

National University Cancer Institute, Singapore (NCIS)〈共催：武田薬品工業株式会社〉

ランチョンセミナー 4
5月12日㈰LS4

第2会場

正博（Masahiro Abe）
（徳島大学大学院 医歯薬学研究部 血液・内分泌代謝内科学分野）

ポスター

座長：安倍

12:10 - 13:00

CD38 の基礎知識を骨髄腫治療に応用する～ダラツムマブの効果を最大限に発揮するために～

19

三原

圭一朗
（Keichiro Mihara）

広島大学病院 造血器診療科 血液内科

〈共催：ヤンセンファーマ株式会社〉

モーニングセミナー

モーニングセミナー 1
5月12日㈰座長：半田MS1

8:00 - 8:40 第1会場
寛（Hiroshi Handa）（群馬大学大学院医学系研究科内科学講座血液内科学分野）

カルフィルゾミブの持つ免疫学特性＝長期使用が可能なプロテアソーム阻害薬＝
Focus on immunological characteristics behind Calfilzomib

伊藤量基（Tomoki Ito）

関西医科大学附属病院 血液腫瘍内科〈共催：小野薬品工業株式会社〉

モーニングセミナー 2
5月12日㈰座長：伊藤MS2

8:00 - 8:40 第2会場
薫樹（Shigeki Ito）
（岩手医科大学 臨床腫瘍学講座）

多発性骨髄腫に対する免疫学的アプローチ
Immunological Approach for Multiple Myeloma萩原

ランチョンセミナー

Apply required knowledge about CD38 for treatment in myeloma patients～ To maximize the power of daratumumab for treatment ～將太郎（Shotaro Hagiwara）

東京女子医科大学 血液内科学講座〈共催：ブリストル・マイヤーズ スクイブ株式会社〉

47

プログラム（Program）

スポンサードシンポジウム1
5月11日㈯

15:20 - 16:50

第1会場

高齢多発性骨髄腫患者の治療
Treatment strategy of elderly multiple myeloma patients
座長：飯田 真介（Shinsuke Iida）（名古屋市立大学大学院医学研究科 血液・腫瘍内科学）
張 高明（Takaaki Chou）（新潟県立がんセンター新潟病院 内科）

SS1-1

高齢多発性骨髄腫患者の治療 - 最適な治療を選択するために考慮すべきこと
Treatment for elderly multiple myeloma patients-What we evaluate for optimizing
therapy?

半田寛（Hiroshi Handa）

群馬大学大学院医学系研究科 内科学講座 血液内科学分野

SS1-2

Emerging treatment options for elderly patients with multiple myeloma

Andrew Spencer

Professor, Department of Clinical Haematology, Alfred Hospital and Monash University

SS1-3

Assessing frailty in older MM patients

Saad Z. Usmani

Clinical Professor of Medicine, UNC School of Medicine, Levine Cancer Institute, Charlotte, NC〈共催：ヤンセンファーマ株式会社 メディカルアフェアーズ本部〉

スポンサードシンポジウム2
5月12日㈰10:20 - 11:50

第1会場

多発性骨髄腫治療におけるMRDの意義
Role of MRD Assessment in Multiple Myeloma
座長：宮本

SS2-1

敏浩（Toshihiro Miyamoto）（九州大学大学院医学研究院病態修復内科学）

Impact of Sustained Minimal Residual Disease (MRD) Negativity in Multiple Myeloma

Hervé Avet-Loiseau

Unite de Genomique du Myelome, CHU Rangueil, Toulouse, France

SS2-2

日本国内における多発性骨髄腫 MRD 測定の現状
Minimal Residual Disease Assessment in Myeloma in Japan髙松博幸（Hiroyuki Takamatsu）

金沢大学医薬保健研究域医学系 血液内科

〈共催：セルジーン株式会社〉48

会長講演（Presidential Lecture）

会長講演（Presidential Lecture）

飯田

会長講演

PL

プレシジョンメディシン時代における多発性骨髄腫治療の展望
Treatment of multiple myeloma in this era of precision medicine: a perspective
真介

Shinsuke Iida

名古屋市立大学大学院医学研究科 血液・腫瘍内科学

Department of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Japan

Recent advances in the development of novel agents such as proteasome inhibitors (PI), immunomodulatory
drugs (IMiDs), and monoclonal antibodies (mAbs) have dramatically improved the prognosis of the patientswith multiple myeloma (MM). Currently, induction therapy with novel agents followed by autologous stemcell transplantation (ASCT) is the standard of care for transplant-eligible patients with newly diagnosed MM(NDMM). For transplant-ineligible patients with NDMM, treatment with novel agents either for the limited
period or as continuous therapy based on the hypothesis that “one size fits all” is the best choice.
On the other hand, MM consists of various heterogeneous diseases based on chromosomal and molecularalterations. Furthermore, subgroup analyses in large-scale clinical trials have revealed different sensitivities
to each novel agent according to subtypes of MM. For instance, long-term use of PIs and IMiDs are
particularly effective for MM patients with high-risk and standard-risk cytogenetics, respectively; mAbs
in combination with these agents can increase their efficacy. In this era of precision medicine, relatively
few cancer patients benefit from implementation of the clinical sequence using next-generation sequence(NGS) and microsatellite instability analysis. In MM, our clinical sequence study has identified potentiallyactionable findings (PAF) associated with subtype diagnosis and prediction of the prognosis in over 60% of
patients, whereas druggable driver gene mutations have been found in this limited number of patients either
due to no available molecular targeting agents being effective for frequently detected driver mutations in
MM such as K-RAS or due to the low variant allele frequencies (VAF) of the druggable mutations. However,
the recent discovery of a Bcl2-specific inhibitor in MM carrying t(11;14) with remarkable activity has
illustrated stratification of MM subtypes in terms of the decision of the treatment strategy. Subtypes of MM
plus patient status such as frailty, complications, organ functions, and presence of absence of caregivers areother important determinants of the treatment choice, especially in elderly patients. Since even novel agentsare associated with various adverse events, now is the time to consider the best treatment strategy according
to MM subtypes and patient status so that stratified or personalized treatment can be developed in the near
future.

51

シンポジウム（Symposium）

シンポジウム（Symposium）

SY1-1

Treatment strategy in high-risk multiple myeloma

Wee Joo Chng
National University Cancer Institute, Singapore

Despite the improvement in outcomes of myeloma patients, the progress in high-risk myeloma has been lagging behind.
The definition of high-risk disease is also evolving: R-ISS stage III, high-risk genetics, double hit myeloma, GEP-definedhigh-risk, are some of the important factors proposed in the literature. However, in most trials, high-risk is defined basedon genetics. While specific trials in high-risk myeloma has been scarce, the have been a number of signals from posthoc analysis of different trials that may provide useful information on how we could potentially improve outcomes ofhigh-risk myeloma patients. An important aspect is understanding the biology of high-risk myeloma and devising novel
approaches to treat these patients. Some insights from this area of research will be shared.

54

シンポジウム（Symposium）

SY1-2
良顕

シンポジウム１

知念

多発性骨髄腫の染色体・ゲノム診断の基礎と展望
Current standard and future perspective of cytogenetic and genetic diagnosis in multiple
myeloma

Yoshiki Chinen

京都府立医科大学 血液内科

Division of Hematology and Oncology, Kyoto Prefectural University of Medicine, Japan

Multiple myeloma (MM) is a cytogenetically/molecularly heterogeneous hematologic malignancy that remains mostly
incurable. Thus, further developments in risk stratification, precision medicine, and response monitoring are important toimprove treatment outcomes for MM.
To date, next-generation sequencing and gene expression profiling have identified many emerging genetic aberrations.
However, the best way to incorporate these abnormalities into clinical practice remains unclear. Genome-wide screening
has revealed gene mutations associated with signal pathways involved in proliferation, survival and drug-resistance ofMM, that could contribute to the development of targeted therapeutics. In contrast, no significant associations have beenfound between individual genomic events and treatment response to proteasome inhibitors or immunomodulatory drugs.
In addition, multi-region sequencing and serial genomic analysis at different disease courses of MM have demonstrated
the spatial and temporal genomic heterogeneity of MM. Furthermore, the frequency of gene mutations increases
significantly in cytogenetically high-risk MM patients vs. standard-risk MM patients. Cytogenetic abnormalities can beused as major prognostic factors compared to gene mutations, and detection of high-risk cytogenetic abnormalities byinterphase fluorescence in situ hybridization (FISH) provides a simple risk stratification algorithm for MM.
In this session, I would like to review the clinical significance of molecular and cytogenetic abnormalities, and discuss
the potential of FISH and genome-wide screening techniques as promising clinical applications in MM.

55シンポジウム（Symposium）

SY1-3
金森

日本人新規診断多発性骨髄腫における網羅的ゲノム解析
Comprehensive genetic analysis of newly diagnosed multiple myeloma in Japan貴之 1,2、眞田昌 2、李政樹 1、飯田真介 1

Takashi Kanamori , Masashi Sanada , Masaki Ri , Shinsuke Iida3
1

2

3

1

名古屋市立大学大学院医学研究科 血液・腫瘍内科学、2国立病院機構名古屋医療センター 高度診断研究部

Department of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Japan, 2Clinical1

Research Center, National Hospital Organization Nagoya Medical Center, Japan

Multiple myeloma (MM) is a genetically heterogeneous disease. The early development of MM is principally mediatedby IGH-translocations and hyperdiploidy, and it progresses into symptomatic MM with additional genetic abnormalities
and chromosomal aberrations.
Recently, next generation sequencing (NGS) technologies have enabled comprehensive analysis of genomic
abnormalities occurring in cancer cells. Now, we have developed and evaluated a platform detecting gene mutation,
structural variant and copy number alteration in purified plasma cells derived from newly diagnosed MM (NDMM)
patients.
So far, whole-exome sequencing of more than 1,000 samples derived from MM patients has been performed andrevealed that almost half of the patients harbored abnormalities of RAS/MAPK pathway genes at initial diagnosis. In
addition, DIS3, which is engaged in the RNA editing, and FAM46C, whose role in MM pathogenesis remains unknown,
are frequently mutated in MM cells in contrast to their rare involvement in other hematological malignancies. However,
the genomic profiles of Asia or Japanese MM patients remain unclear.
We performed comprehensive genetic analysis of 138 samples derived from Japanese NDMM patients using targetedcapture sequencing. While most of these results were compatible with previous reports, we found out that hyperdiploidy
was less frequent and KRAS mutation was more frequent than previously reported.
In this symposium, an overview of the genetic features of MM cells using NGS including those in Japanese MMpatients is going to be presented. Further delineation of each genetic alteration is expected to predict either more precise
prognosis of the patients or response to specific therapeutic agents in near future.

56

シンポジウム（Symposium）

SY1-4
鈴木

多発性骨髄腫における染色体異常と治療戦略
Treatment strategy stratified with cytogenetic abnormality in multiple myeloma

一史

シンポジウム１

Kazuhito Suzuki

東京慈恵会医科大学附属柏病院 腫瘍・血液内科

Clinical Oncology/ Hematology, The Jikei University Kashiwa Hospital, Japan

Multiple myeloma (MM) comprises a heterogeneous group of plasma cell neoplasms and remains incurable diseasealthough the development of novel agents, such as proteasome inhibitors (PI), immunomodulatory drugs (IMiDs)
and monoclonal antibodies have improved its prognosis over the last decade. Risk stratification using cytogenetic
abnormality might be essential but has not performed commonly in real world practice until now. I will present treatment
strategy stratified with cytogenetic abnormality including t(4;14), del17p, and t(11;14). t(4;14) is detected about 15% of
MM patients and one of high risk abnormality and overexpresses MMSET. PI improves outcome in MM patients witht(4;14) according to several prospective studies. SLAMF7 is regulated by MMSET and expressed on cell surface inhuman myeloma cell lines with t(4;14). Elotuzumab, monoclonal anti-SLAM7 antibody, might be active for MM patientswith t(4;14). Del17p is one of the most important cytogenetic abnormalities because del17p showed negative impact ofsurvival in many clinical trials. In attention, the cutoff value of del17p using FISH is controversial. Del17p are detected
in about 10% at diagnosis and increases up to 80% in later stage. TP53 gene, which is one of tumor suppressor gene, ismapped at 17p13. However, del17p is not always identified with mutation of TP53. TP53 related protein kinase (TP53RK)
regulates p53 activity. Pomalidomide downregulates TP53RK and is active in MM patients with del17p. t(11;14) is
detected 15-20% of MM patients and not identified with high risk cytogenetic abnormality. However, survival in MM
patients with t(11;14) was shorter than those with other standard risk. Triplet regimens improve outcome in MM patientswith t(11;14) according to a retrospective study. Venetoclax, which is a BCL2 inhibitor, is active in MM patients witht(11;14) compared with those without t(11;14). Activity of venetoclax is associated with high Bcl-2 and low Mcl-1/BclXL. These molecule subgroups was detected frequently in MM patients with t(11;14).

57

シンポジウム（Symposium）

SY2-1

Therapeutic Strategies for Multiple Myeloma with Renal Impairment

Sundar Jagannath
Mount Sinai Hospital, New York, NY, USA

Renal impairment (RI) is a common complication of multiple myeloma (MM). About 20–30% of patients with MM
are diagnosed with RI, of whom ~10% require hemodialysis. In most cases, RI is caused by the accumulation andprecipitation of light chains, which form casts in the distal tubules and cause renal obstruction. Additionally, MM lightchains are directly toxic on proximal renal tubules, further adding to renal dysfunction. RI is associated with poor
prognosis, and management of MM patients presenting with renal disorders requires rapid control of the disease to avoid
long term sequalae. Conventional chemotherapy for MM has limitations in patients with RI due to increased likelihoodof toxicities or a need for dose reductions. MM prognosis with RI has steadily improved since the introduction of novel
agents. Once patients with RI achieve a remission, their outcomes are similar to patients without RI. For example,
clinical studies that have included newly diagnosed and refractory patients indicate that bortezomib- and IMiD agent +proteasome inhibitor-based regimens may result in rapid reversal of renal failure in up to 50% of patients. Monoclonal
antibodies that are not cleared by the kidneys and do not typically require dose modification in this setting are particularly
attractive. An understanding of the pharmacokinetic properties of individual drugs along with their safety and efficacy
are important considerations when selecting therapy. We will review important considerations for this patient population,
including optimal supportive care and definitive therapy.

58

シンポジウム（Symposium）

SY2-2
淵田

アミロイドーシス合併骨髄腫患者の治療
Treatment of multiple myeloma complicated with AL amyloidosis

真一

Shin-ichi Fuchida

JCHO京都鞍馬口医療センター 血液内科

Department of Hematology, JCHO Kyoto Kuramaguchi Medical Center, Japan59

シンポジウム２

While 12-15% of patients with multiple myeloma (MM) develop overt clinical AL amyloidosis through the courseof disease, up to 30% of myeloma patients are found to have subclinical amyloid deposits. MM associated with AL
amyloidosis (MM/AL) represents a poorer prognosis disease even in the absence of symptoms at diagnosis. The presenceof symptomatic amyloidosis clearly worsens their prognosis.
AL amyloidosis patients have a much higher potential for treatment-related mortality due to underlying organ
dysfunction, therefore it is necessary to take into account several factors such as cardiac, renal, gastrointestinal andhepatic dysfunction as well as peripheral neuropathy in the treatment of MM/AL. Especially, cardiac amyloidosis is
one of the most important risk factors for transplant-eligible patients, so the patient selection for transplantation should
be carefully considered according to the eligibility criteria, and the dose-adjustment of melphalan for conditioning isrequisite according to the recommendation by Comenzo and Gertz. In addition, toxicity of chemotherapeutic drugs
should be considered in AL amyloidosis patients because the use of anti-cancer drugs can cause further damage tothe underlying organ dysfunction. For example, cyclophosphamide, doxorubicin, and bortezomib are toxic for heart,bortezomib and thalidomide for nervous systems, and melphalan and lenalidomide for kidney.
In summary, the treatment of MM/AL has increased risk of adverse events and treatment related complications, therefore
treatment should be planned to minimize toxicity.

シンポジウム（Symposium）

SY2-3
安倍

骨髄腫骨病変治療の進歩と展望
Current status and future perspective of the treatment for myeloma bone disease

正博

Masahiro Abe

徳島大学大学院医歯薬学研究部 血液・内分泌代謝内科学分野

Department of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School, Japan

Multiple myeloma develops and expands almost exclusively in the bone marrow, and generates devastating bone
destruction. A variety of cytokines are overproduced in myeloma to stimulate RANKL-mediated osteoclastogenesis
while suppressing osteoblastic differentiation from bone marrow stromal cells, leading to extensive bone destruction
with rapid loss of bone. Despite recent great strides achieved in myeloma treatment owing to the implementation of new
anti-myeloma agents, bone destruction still remains a leading cause for deterioration in quality of life (QoL) in patientswith myeloma. Of note, aggressive bone destruction has been still negatively impacting their prognosis in terms ofsurvival even in the era of new agents. With improvement of survival in the great majority of patients with myeloma,
bone management will become more important for maintaining the QoL; novel treatment modalities with bone anabolic
activity are highly wanted to restore bone in bone destructive lesions aside from the prevention of bone destruction
with currently available anti-resorptive agents. Novel therapeutic neutralizing antibodies against DKK-1 or sclerotin
are expected as bone anabolic agents; however, their effects on myeloma tumor progression through activation of the
Wnt/β-catenin pathway remain to be carefully clarified. Long-term management for myeloma bone disease and cancer
treatment-induced bone loss should be adequately integrated in the evolving anti-myeloma treatment paradigm.

60

シンポジウム（Symposium）

SY3-1
Andrew Spencer
Department of Clinical Haematology, Alfred Hospital, Melbourne, Australia

シンポジウム２
シンポジウム３61シンポジウム（Symposium）

SY3-2
藤原

骨髄腫関連腫瘍抗原を認識する受容体遺伝子を導入した T 細胞を用いる治療抵抗性骨髄腫に対する養子免疫療法
Adoptive cellular immunotherapy against refractory myeloma using engineered T cells to
express receptor for myeloma-associated tumor antigen

弘

Hiroshi Fujiwara

三重大学 大学院医学系研究科

個別化がん免疫治療学分野

Department of Personalized Cancer Immunotherapy, Mie University, Graduate School of Medicine, Japan

Although, in this century, development of new drugs has brought a dramatic success in the treatment of multiple
myeloma (MM), MM still remains incurable. Notably, patients with relapsed/refractory (r/r) MM have a poor prognosis.
In this context, adoptive cellular immunotherapy (ACI) using engineered T cells to express receptor for myelomaassociated tumor antigen against r/r MM has emerged. First, an ACI using T-cell receptor gene modified autologous T
cells targeting NY-ESO-1, a cancer-testis antigen expressed by myeloma cells in the context of HLA-A*02:01 (NY-ESO-1/
TCR-T) has clinically been introduced. Then, the recent great success in the treatment of r/r B-cell malignancies using
chimeric antigen receptor gene-modified autologous T cells targeting B-cell differentiation antigen CD19 (CD19-CAR-T)
has similarly accelerated this trend for r/r MM. Currently, CAR-T cell therapy against r/r MM has been being developed
centering around B-cell maturation antigen (BCMA), which has demonstrated a great promise. Clinical trials alreadyhave been conducted notably in U.S. and China. Meanwhile, issues to be addressed including cytokine release syndrome
and relapse have become defined in analogy with CD19-CAR-T. Aiming at further clinical efficacy, exploration of new
therapeutic targets other than BCMA, development of more effective CAR gene construct and combined strategies using
other therapeutic agents have also been under investigation.
Taken together, in this presentation, I would like to overview current status and future prospect of this fast-evolving field.

62シンポジウム（Symposium）

SY3-3
水野

造血器腫瘍のプレシジョンメディシン：多発性骨髄腫における現状とこれから
Precision medicine in hematological malignancies: current status in multiple myeloma

晋一

Shinichi Mizuno

九州大学 医学研究院保健学部門検査技術学分野

Division of Medical Sciences and Technology, Department of Health Sciences, Faculty of Medical Sciences, Kyushu University,
Japan

63

シンポジウム３

The current concept of precision medicine in oncology is to link actionable gene mutations to potential therapeutic
agents, and has been proved to be a promising approach in various types of tumors. In Japan, cancer genome medicine
has also been implemented, and is finally set to be provided under the national health insurance system with approved
NGS-based gene panels designed for solid tumors in this 2019. In hematological malignancies, targeted gene panels
are in preparation as well and more detailed clinical applications of genomic medicine are highly required. In precision
medicine, hematology has been a front-runner with the first molecular targeted therapies of all-trans retinoic acid for APL
and imatinib for CML followed by the development of a large number of therapeutic agents for tumors, and the progressin hematology continues to pave the way for the next generation of precision medicine in the coming ear of omicsbased integrated approaches to cancer profiling. In this presentation, I will review the precision medicine in hematology
focusing on multiple myeloma with introduction of our developed clinical sequencing panel for linking genetic diagnosis
with molecular target agents in hematological malignancies. In addition, emerging applications of artificial intelligence(AI) in precision medicine will also be discussed.

Pros and Cons

Pros and Cons

PC-1
上村

自家移植後の維持療法は行うべきである
Maintenance therapy is necessary for patients with MM following ASCT智彦

Tomohiko Kamimura

原三信病院 血液内科

Department of Hematology, Harasanshin Hospital, Japan

In the era of novel agents, maintenance therapy is expected to prolong PFS and OS with less toxicity. Two main studies
conducted by IFM and CALGB showed that lenalidomide (Len)-maintenance improved PFS, whereas a significant
improvement in OS was noted in the CALGB study only. A pooled meta-analysis demonstrated that Len-maintenanceprolonged both PFS and OS. However, these studies were limited by the variety in induction therapy. There isconsiderable evidence of the efficacy of Len-maintenance in a large prospective randomized study in Myeloma XI,
showing a significant increase in PFS and OS (3-year OS, 87.5% vs 80.2%) in transplanted patients. Interestingly, PFS
was also beneficial in high-risk cytogenetics patients (HRC). Also, Len-maintenance improves PFS2, and subsequent
OS is comparable with that in patients without maintenance therapy, whereas thalidomide maintenance appears to
reduce post-relapse survival. However, an increased risk of secondary primary malignancies (SPMs) has been observedin MM patients, particularly after Len-maintenance. Recently, a pooled meta-analysis revealed that patients with Lenmaintenance had lower risk of death but a higher risk of SPMs. The marked improvement of survival outweighs
complications, such as infections and hematologic toxicities, most of which can be managed by dose reduction andsymptomatic therapy. Finally, although the benefit of Proteasome inhibitor-based maintenance has not been clearly
established, maintenance with bortezomib or ixazomib could improve PFS with HRC, including 17p deletion.

66

Pros and Cons

PC-2
尾崎

自家移植後の維持療法は全例に必要か？
Should all patients receive maintenance therapy after autologous stem cell transplantation?

修治

Shuji Ozaki

徳島県立中央病院 血液内科

Department of Hematology, Tokushima Prefectural Central Hospital, Japan

67

Pros and Cons

The treatment of young or transplant-eligible multiple myeloma patients mostly consists of autologous stem celltransplantation (ASCT) as the most powerful consolidation therapy after induction. However, the majority of patients
eventually relapse even after ASCT, and maintenance or continuous therapy has been used for long-term disease control.
Maintenance therapy should prevent disease progression and improve overall survival without causing adverse events
that could lead to a decreased quality of life. Recently, low-dose, single agent lenalidomide has been studied extensively
as maintenance or continuous therapy in both transplant-eligible and -ineligible patients. Several large randomized trials
have demonstrated a significant prolongation of progression-free survival and a modest survival benefit in transplanted
and non-transplanted patients who received lenalidomide maintenance. Therefore, maintenance with lenalidomide isconsidered as the standard of care for every newly diagnosed patient. However, there are some issues to be overcome formaintenance therapy in order to become widely accepted in routine clinical practice. As previous studies have shown,
the efficacy of lenalidomide is rather limited in the subgroup of patients harboring high-risk cytogenetic abnormalities.
There are also concerns about long-term toxicity, high treatment costs, and the possibility of selection of resistant clones.
Currently, more effective agents that induce deeper responses are available, and an optimal treatment strategy should beestablished for each patient.

プレナリー（Plenary）

プレナリー（Plenary）

PL1-1

Phase 3 Study of Daratumumab Plus Lenalidomide and Dexamethasone (D-Rd) Vs. Rd in
Transplant-ineligible
Phase 3 Study of Daratumumab Plus Lenalidomide and Dexamethasone (D-Rd) Vs. Rd in
Transplant-ineligible Newly Diagnosed Multiple Myeloma (NDMM): MAIA

Saad Usmani1, Shaji K. Kumar2, Torben Plesner3, Robert Z. Orlowski4, Philippe Moreau5, Nizar Bahlis6,

Supratik Basu7, Hareth Nahi8, Cyrille Hulin9, Hang Quach10, Hartmut Goldschmidt11, Michael O’Dwyer12, Aurore Perrot13,
Christopher P. Venner14, Katja Weisel15, Joseph R. Mace16, Tahamtan Ahmadi17, Christopher Chiu18, Jianping Wang19,

Rian van Rampelbergh20, Clarissa M. Uhlar18, Rachel Kobos19, Ming Qi18, Thierry Facon21

Levine Cancer Institute/Atrium Health, Charlotte, NC, USA, 2Department of Hematology, Mayo Clinic Rochester, Rochester, MN,

1

USA, 3Vejle Hospital and University of Southern Denmark, Vejle, Denmark, 4Department of Lymphoma and Myeloma, Universityof Texas M.D. Anderson Cancer Center, Houston, TX, USA, 5Hematology, University Hospital Hôtel-Dieu, Nantes, France,

University of Calgary, Arnie Charbonneau Cancer Institute, Calgary, AB, Canada, 7Royal Wolverhampton Hospitals NHS Trust,

6

Wolverhampton, United Kingdom, 8Karolinska Institute, Department of Medicine, Division of Hematology, Karolinska University
Hospital at Huddinge, Stockholm, Sweden, 9Department of Hematology, Hospital Haut Leveque, University Hospital, Pessac,
France, 10St. Vincent's Hospital, University of Melbourne, Melbourne, Australia, 11University Hospital Heidelberg and National

Center of Tumor Diseases (NCT), Heidelberg, Germany, 12Dept. of Medicine/Haematology, NUI, Galway, Ireland, 13Hematology

Department, University Hospital, Vandoeuvre Les Nancy, France, 14Division of Medical Oncology University of Alberta,

Edmonton, AB, Canada, 15Universitaetsklinikum Tuebingen der Eberhard-Karls-Universitaet, Abteilung fuer Innere Medizin II,

Tuebingen, Germany, 16Florida Cancer Specialists & Research Institute, St. Petersburg, FL, USA, 17Genmab US, Inc., Princeton, NJ,

USA, 18Janssen Research & Development, Spring House, PA, USA, 19Janssen Research & Development, Raritan, NJ, USA, 20Janssen

Research & Development, Beerse, Belgium, 21Service des Maladies du Sang, Hôpital Claude Huriez, Lille, France

Lenalidomide-based therapies are standard of care (SoC) for transplant-ineligible (TIE) NDMM pts. Daratumumab (D)is an anti-CD38 mAb with single-agent activity in heavily pretreated MM. Based on the efficacy and safety profile of
D-Rd in relapsed or refractory MM, we conducted a phase 3 study (MAIA) to evaluate D-Rd vs Rd in TIE NDMM.
Pts ineligible for high-dose chemotherapy + ASCT were randomized to receive 28-day cycles of treatment with Rd ±D. R: 25 mg PO QD on Days 1‑21; d: 40 mg PO on Days 1, 8, 15 and 22 ± D:16 mg/kg IV QW for Cycles 1‑2, Q2W
for Cycles 3-6, and Q4W thereafter. Primary endpoint was PFS. The prespecified interim analysis was conducted after
240 PFS events among 737 randomized pts (D-Rd, 368; Rd, 369) at a median follow-up of 28 mo. Median PFS for
Rd was 31.9 mo vs not reached for D-Rd (HR, 0.56; 95% CI, 0.43-0.73; P<0.0001). D-Rd resulted in higher rates ofdeeper responses (≥CR: 47.6% vs 24.9%; ≥VGPR: 79.3% vs 53.1%; both P <0.0001). In total, 19% of pts died (OS HR,
0.78; 95% CI, 0.56-1.1); follow-up is ongoing. Higher rates (≥5% difference) of grade 3/4 pneumonia, neutropenia, andleukopenia were observed with D-Rd, consistent with previously reported studies. The complete topline data set will bepresented. D-Rd significantly reduced the risk of progression or death by 44%, with no new safety signals in TIE NDMM
pts. These data along with the phase 3 ALCYONE study (D + bortezomib/melphalan/prednisone [VMP] vs VMP)
support daratumumab + SoC in TIE NDMM.

70

プレナリー（Plenary）

PL1-2

多発性骨髄腫における有糸分裂チェックポイントタンパク BUB1 高発現の機能的意義
Functional significance of Mitotic Checkpoint Protein BUB1 Overexpression in Multiple
Myeloma

藤林 悠人 1、坂元 - 稲田 奈津美 1、桑原 - 太田 沙絵子 1、伊佐 怜子 1、山口 順子 1、西山
松村 - 木元 弥生 1、知念 良顕 1、志村 勇司 1、古林 勉 1、谷脇 雅史 2、黒田 純也 1

大地 1、

Yuto Fujibayashi1, Natsumi Sakamoto-Inada1, Saeko Kuwahara-Ota1, Reiko Isa1, Junko Yamaguchi1, Daichi Nishiyama1,

Yayoi Matsumura-Kimoto1, Yoshiaki Chinen1, Yuji Shimura1, Tsutomu Kobayashi1, Masafumi Taniwaki2, Junya Kuroda1
1

京都府立医科大学大学院医学研究科 血液内科学、2京都府立医科大学大学院分子診断・治療センター

Division of Hematology and Oncology, Department of Medicine, Kyoto prefectural University of Medicine, Graduate School of

1

Medical Science, Japan, 2Center for Molecular Diagnostics and Therapeutics, Kyoto Prefectural University of Medicine, Graduate

School of Medical Science, Japan

71

プレナリー１

Clonal evolution due to chromosomal instability (CIN) is the major driving force of the disease progression in multiple
myeloma (MM). However, the mechanisms underlying CIN remains to be unclear in MM. Faithful chromosomal
segregation is tightly regulated by coordinated functions of mitotic checkpoint proteins. BUB1 is one of mitotic
checkpoint proteins, and its high expression has been associated with poor prognosis in several types of cancers.
However, the exact mechanisms by which BUB1 affects cell phenotype are unknown in MM. We in this study identified
that BUB1 mRNA expression was significantly higher in patient-derived myeloma cells compared to that in normal
plasma cells. Moreover, BUB1 expression level was found to be significantly higher in myeloma cells from advanced
stage than that in myeloma cells of early stage. Intriguingly, gene knockdown of BUB1 using lentivirus-mediated RNAinterference targeting BUB1 caused the reduced chromosome segregation abnormalities, such as chromosomal break,bridge or lagging, in two human myeloma-derived cell lines, KMS-18 cells and AMO-1 cells, while did not impair cellproliferation or cell survival. In addition, BUB1 knockdown reduced colony-forming ability of KMS-18 cells. Thesesuggest that enhanced BUB1 expression associates with the increase of clones those are prone to acquire chromosomal
abnormality by CIN with increased mitotic segregation error in MM. Further studies elucidating function and regulatory
mechanism of BUB1 may contribute to development of novel treatment strategy which can prevent clonal evolution inMM.

プレナリー（Plenary）

PL1-3
長谷川

多発性骨髄腫細胞で小胞体ストレス下において発現する CD98 は抗体療法の特異的標的となる
CD98 turns into a specific therapeutic target under endoplasmic reticulum stress in multiple
myeloma加奈、保仙直毅

Kana Hasegawa, Naoki Hosen

大阪大学大学院 医学系研究科 癌幹細胞制御学寄附講座

Department of Cancer Stem Cell Biology, Osaka University Graduate School of Medicine, Japan

Cancer-specific cell surface antigens are ideal therapeutic targets1-5. However, most transcripts or proteins highly specificfor cancer cells are likely to have already been identified after extensive efforts using transcriptome or proteome analyses.
Here, we report that a protein broadly expressed on normal cells can turn into a cancer-specific therapeutic target under
endoplasmic reticulum (ER) stress in multiple myeloma (MM). We screened more than 10,000 monoclonal antibody(mAb) clones raised against MM cells, and identified R8H283 as a mAb that bound to MM cells but not to normal
hematopoietic cells. R8H283 specifically recognized CD98, which is expressed on all normal leukocytes, indicatingthat it reacts with only a subset of CD98 protein. Induction of ER stress, which commonly occurs in MM cells, caused
expression of the R8H283 antigen, most likely via a reduction in glycosylation of the CD98 protein. R8H283 exerted
significant anti-MM effects without damaging normal hematopoietic cells. These findings not only show that R8H283
is a promising candidate for as an anti-MM therapeutic mAb, but also suggest that cancer-specific antigen epitopes may
also be identified in other types of cancer cells undergoing ER stress, even if expression of the proteins themselves is notcancer-specific.

72

プレナリー（Plenary）

PL1-4

未治療多発性骨髄腫における末梢血 cell free DNA 解析
Analysis of serum cell free DNA in patients with multiple myeloma

立田 卓登 1、李 政樹 1、青木 奨 1、浅野 有彩 1、金森 貴之 1、戸谷 治仁 1、木下
成田 朋子 1、正木 彩子 2、伊藤 旭 1、楠本 茂 1、小松 弘和 1、飯田 真介 1

史緒理 1、浅尾

優 1、Takuto Tachita1, Masaki Ri1, Sho Aoki1, Arisa Asano1, Takashi Kanamori1, Haruhito Totani1, Shiori Kinoshita1, Yu Asao1,
Tomoko Narita1, Ayako Masaki2, Asahi Ito1, Shigeru Kusumoto1, Hirokazu Komatsu1, Shinsuke Iida1

1

名古屋市立大学大学院医学研究科 血液・腫瘍内科学、2名古屋市立大学大学院医学研究科 臨床病態病理学

Department of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Japan, 2Department

1of Pathology and Molecular Diagnostics, Nagoya City University Graduate School of Medical Sciences, Japan73

プレナリー１

Multiple myeloma (MM) is considered as the clonally diverse disease. Although extramedullary disease (EMD) biopsy
and bone marrow (BM) aspiration uncover intra-patient genetic heterogeneity of MM clones, frequent testing of theseprocedures is not easily acceptable. Thus, we focused on the cell free DNA (cfDNA) as an alternative way to detect
genetic heterogeneity of MM cells. Eighty-one serum samples from the patients with newly diagnosed MM (NDMM)
were subjected to the quantitative analysis of cfDNA. Detection of genetic mutations in serum cfDNA was applied tothe two NDMM patients harboring high-risk karyotype, and compared them with those of BM plasma cells (BMPC)
using the human comprehensive cancer panels (275 genes). Amount of serum cfDNA was significantly higher in patientswith NDMM (median 78.1ng/mL) than healthy volunteers (n=10, median 31.6ng/mL). The amount of serum cfDNA
showed a weak correlation with the level of serum monoclonal free light chains. In terms of genetic mutations, twopatients respectively possessed 78 and 158 mutations in cfDNA and the numbers of the mutations were more than thoseof the BMPCs, i.e., 19 and 21, respectively. Approximately 80% of mutations detected in BMPCs were also observed inserum cfDNA. Moreover, various unique mutations not observed in BMPCs were detected in serum cfDNA. Our results
suggest that serum cfDNA analysis sufficiently covers critical mutations in BMPCs, and may detect the unique mutationsin EMD. The cfDNA analysis would be an alternative choice for detecting the mutational landscape of whole body MM
cells.

プレナリー（Plenary）

PL1-5

造血幹細胞移植後の初発の多発性骨髄腫患者におけるイキサゾミブ維持療法による無増悪生
存期間の延長：TOURMALINE MM3 試験
Ixazomib Maintenance Post-Transplant Significantly Prolongs Progression-Free Survival in
Newly Diagnosed Multiple Myeloma: The TOURMALINE-MM3 Trial

Wee-Joo Chng1, Meletios A Dimopoulos2, Francesca Gay3, Fredrik H Schjesvold4, Meral Beksac5, Roman Hajek6,

Katja C Weisel7, Hartmut Goldschmidt8, Vladimir Maisnar9, Philippe Moreau10, Chang Ki Min11, Agnieszka Pluta12,

Martin Kaiser13, Sonja Zweegman14, Maria Victoria Mateos15, Andrew Spencer16, Shinsuke Iida17, Gareth J Morgan18,

Kaveri Suryanarayan19, Zhaoyang Teng20, Tomas Skacel21, Antonio Palumbo21,22, Ajeeta B Dash23, Neeraj Gupta24,
Richard Labotka19, S Vincent Rajkumar25

Department of Haematology-Oncology, National University Cancer Institute, National University Health System, Singapore,
and Cancer Science Institute of Singapore, National University of Singapore, Singapore, 2Hematology and Medical Oncology,

1

Department of Clinical Therapeutics, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece,

Department of Oncology and Hematology, Azienda Ospedaliero-Universitaria City of Health and Science of Turin, Turin,
Italy, 4Oslo Myeloma Center, Oslo University Hospital, Oslo, Norway, and KG Jebsen Center for B cell malignancies, Universityof Oslo, Oslo, Norway, 5Department of Hematology, Ankara University, Ankara, Turkey, 6Department of Hematooncology,

3

University Hospital Ostrava, Ostrava, Czech Republic, 7Department of Internal Medicine II, University Hospital Tübingen,

Tübingen, Germany, 8Department of Internal Medicine V, University Medical Hospital Heidelberg and National Center ofTumor Diseases, Heidelberg, Germany, 9Fourth Department of Medicine – Hematology, University Hospital Hradec Králové,

Hradec Králové, Czech Republic, 10Department of Hematology, University Hospital Hôtel-Dieu, Nantes, France, 11Department

of Internal Medicine, Seoul St. Mary's Hospital, Seoul, South Korea, 12Department of Hematology, Medical University of Lodz,
Multidisciplinary Provincial Centre of Traumatology and Oncology Nicolas Copernicus in Lodz, Lodz, Poland, 13Departmentof Haematology, The Royal Marsden Hospital, London, UK, and Division of Molecular Pathology, The Institute of Cancer
Research ICR, London, UK, 14Department of Hematology, Amsterdam University Medical Center, VU University Amsterdam,
Cancer Center Amsterdam, Amsterdam, Netherlands, 15Department of Hematology, University Hospital of Salamanca, CIC,

IBMCC, Salamanca, Spain, 16Malignant Haematology and Stem Cell Transplantation Service, Alfred Health-Monash University,
Melbourne, VA, Australia, 17Department of Hematology and Oncology, Nagoya City University Graduate School of Medical

Sciences, Nagoya, Japan, 18Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA, 19Oncology

Clinical Research, Millennium Pharmaceuticals, Inc., a wholly owned subsidiary of Takeda Pharmaceutical Company Limited,
Cambridge, MA, USA, 20Biostatistics, Millennium Pharmaceuticals, Inc., a wholly owned subsidiary of Takeda Pharmaceutical

Company Limited, Cambridge, MA, USA, 21Global Medical Affairs, Millennium Pharmaceuticals, Inc., a wholly owned subsidiaryof Takeda Pharmaceutical Company Limited, Cambridge, MA, USA, 22Myeloma Unit, Division of Hematology, University ofTorino, Azienda Ospedaliero-Universitaria S Giovanni Battista, Turin, Italy, and Center for Hematology and Oncology, University
Hospital Zürich, Zürich, Switzerland, 23Translational Medicine, Millennium Pharmaceuticals, Inc., a wholly owned subsidiaryof Takeda Pharmaceutical Company Limited, Cambridge, MA, USA, 24Drug Metabolism and Pharmacokinetics, Millennium

Pharmaceuticals, Inc., a wholly owned subsidiary of Takeda Pharmaceutical Company Limited, Cambridge, MA, USA, 25Divisionof Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA

Maintenance therapy post-transplant can prolong disease control and survival in newly diagnosed multiple myeloma(NDMM). Lenalidomide is approved for this indication in the US/EU, but is associated with second primarymalignancies (SPMs); bortezomib‑based maintenance shows promising activity post-transplant, but has tolerability/
administration limitations in the real world. More tolerable, convenient options are required. In the double-blind, placebocontrolled TOURMALINE-MM3 study (NCT02181413), NDMM pts with ≥partial response to proteasome inhibitor
and/or immunomodulatory drug-based induction plus single transplant were randomized (3:2) to ixazomib (n=395) orplacebo (n=261) for ~24 mo or until progressive disease/toxicity. Primary endpoint was progression-free survival (PFS).
At a median follow-up of 31 mo (54% of PFS events), there was a 39% PFS improvement with ixazomib vs placebo(median PFS 26.5 vs 21.3 mo; hazard ratio 0.72; 95% CI 0.58–0.89; p=0.0023). Ixazomib led to higher rates of deepened
response vs placebo (46% vs 32%); 12% vs 7% of pts converted from minimal residual disease-positive to -negative
status. With ixazomib vs placebo, 7% vs 5% of pts discontinued treatment due to adverse events (AEs); 42% vs 26% had
grade ≥3 AEs (the most common were infections [15% vs 8%], gastrointestinal disorders [6% vs 1%] and neutropenia [5%vs 3%]); 27% vs 20% had serious AEs; 1 vs 0 pts died on‑study. SPM rate was 3% in both arms. Ixazomib maintenanceis a valuable option in responding pts post‑transplant, with a favorable safety profile and convenient oral dosing.

74プレナリー（Plenary）

PL2-1

多発性骨髄腫における骨髄由来抑制系細胞誘導の分子メカニズムに対する IMiDs の効果
Potency of immunomodulatory drugs in interfering molecular mechanisms underlying theinduction of myeloid-derived suppressor cell in multiple myeloma

太田 沙絵子 1、志村 勇司 1、伊佐 怜子 1、山口 順子 1、西山 大地 1、藤林 悠人 1、下村 とも子 1、水野木元 弥生 1、塚本 拓 1、知念 良顕 1、古林 勉 1、堀池 重夫 1、谷脇 雅史 2、黒田 純也 1

芳美 1、

Saeko Kuwahara-Ota1, Yuji Shimura1, Reiko Isa1, Junko Yamaguchi1, Daichi Nishiyama1, Yuto Fujibayashi1,

Tomoko Takimoto-Shimomura1, Yoshimi Mizuno1, Yayoi Matsumura-Kimoto1, Taku Tsukamoto1, Yoshiaki Chinen1,
Tsutomu Kobayashi1, Shigeo Horiike1, Masafumi Taniwaki2, Junya Kuroda1

1

京都府立医科大学大学院医学研究科 血液内科学、2京都府立医科大学大学院分子診断・治療センター

Division of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Japan, 2Center

1for Molecular Diagnostics and Therapeutics, Kyoto Prefectural University of Medicine, Japan

プレナリー１

The increase of myeloid-derived suppressor cells (MDSCs) those potently impair systemic immune-mediated tumor
surveillance mechanism has been associated with disease progression and treatment resistance in multiple myeloma(MM). This study investigated the molecular mechanisms underlying MDSC induction, and sought to discover strategy
to prevent MDSC induction in MM. By using transwell co-culture system, we identified that two of six human myelomaderived cell lines (HMCLs) examined were potent in inducing CD14+/CD33+/HLA-DR- monocytic (M)-MDSCs fromperipheral blood mononuclear cells (PMNCs) from healthy donor. By analyzing soluble factors derived from MDSCinducible and MDSC-non-inducible HMCLs, CCL5 was found to be secreted only by MDSC-inducible HMCLs, while
MIF was from all HMCLs examined. Addition of anti-CCL5 neutralizing antibody or MIF inhibitor blocked MDSCs
induction, while the supplementation of CCL5 in conditioned medium from MDSC-non-inducible HMCLs was potent in
inducing MDSCs. The combinatory secretion of CCL5 and MIF by myeloma cells was identified to be the prerequisite
for the induction of M-MDSCs. Among moieties currently available for MM, we identified that immunomodulatory
drugs (IMiDs) were found to possess suppressive effects on MDSC induction. IMiDs reduced CCL5 at mRNA levelin MM cells, increased mRNA level of IRF8 and reduced the expression of CCR5, a receptor of CCL5, in PMNCs,
and blocked MDSC differentiation from PMNCs. Our study may give new insights on monitoring the effects ofimmunochemotherapy and the development of new therapy.

プレナリー２75

プレナリー（Plenary）

PL2-2
石橋

免疫調節薬は骨髄腫細胞の PD-L1 発現誘導により T 細胞抑制するが、durvalumab との併用で解除できる
Immunomodulatory drug-induced T-cell suppression via PD-L1 upregulation on myeloma
cells is recovered by durvalumab

真理子 1、山本

淳一 2、伊藤拓水 2、半田宏 2、猪口孝一 3、田村秀人 3

Mariko Ishibashi1, Junichi Yamamoto2, Takumi Ito2, Hiroshi Handa2, Koiti Inokuch3, Hideto Tamura3
1

日本医科大学微生物学・免疫学、2東京医科大学ナノ粒子先端医学部講座、3日本医科大学血液内科

Department of Microbiology and Immunology, Nippon Medical School, Japan, 2Department of Nanoparticle Translational

1

Research, Tokyo Medical University, Japan, 3Department of Hematology, Nippon Medical School, Japan

Introduction: PD-L1 on multiple myeloma (MM) cells not only suppresses tumor-specific cytotoxic T cells but also
induces a high malignant potential via PD-L1–PD-1 interaction. We investigated the regulation of PD-L1 expression
by immunomodulatory drugs (IMDs) and antimyeloma effects of the anti-PD-L1 antibody durvalumab (DUR) in
combination with IMDs.
Methods: 1) PD-L1 expression in MM cell lines and plasma cells from MM patients was analyzed using flow cytometry.
2) PD-L1 induction by IMDs was evaluated based on promoter activity in the luciferase assay. 3) Stable knockdown
MM cells were established using the lentiviral shRNA system. 4) T-cell proliferation was assessed using the CFSE cell
division assay.
Results: 1) PD-L1 expression in MM cell lines and primary MM cells from refractory/relapsed patients was enhanced
by lenalidomide (LEN)/pomalidomide (POM), as confirmed by an increase in PD-L1 promoter activity in HeLa cells.
PD-L1 induction was not seen in cereblon-knockdown MM cells. PD-L1 on Ikaros-knockdown MM cells increased andwas strongly enhanced by LEN/POM. PD-L1 expression in MM cells engrafted in NOG mice was also upregulated by
LEN treatment. 2) The proliferation of T cells co-cultured with LEN/POM-treated MM cells (PD-L1-upregulated cells)
was inhibited in comparison with untreated cells. This inhibition of T cells was prevented more effectively by combined
LEN/POM and DUR treatment compared with DUR alone.
Conclusions: Our study suggests that DUR combined with IMDs may be a reasonable treatment for relapsed/refractory
MM patients.

76プレナリー（Plenary）

PL2-3

Connect® MM registry: Impact of initial treatment on HRQoL and outcomes in newly
diagnosed multiple myeloma without intent for immediate transplant:

Rafat Abonour1, Robert M Rifkin2, Cristina Gasparetto3, Kathleen Toomey4, Brian G. M. Durie5, James W. Hardin6,

Howard R. Terebelo7, Sundar Jagannath8, Mohit Narang9, Sikander Ailawadhi10, Shankar Srinivasan11, Liang Liu11,
Amani Kitali11, Amit Agarwal11, Lynne Wagner12

Indiana University, Indianapolis, IN, USA, 2Rocky Mountain Cancer Centers US Oncology, Denver, CO, USA, 3Duke University

1

Medical Centre, Durham, NC, USA, 4Steeplechase Cancer Center, Somerville, NJ, USA, 5Cedars-Sinai Medical Center, Los Angeles,

CA, USA, 6University of South Carolina, Columbia, SC, USA, 7Providence Cancer Institute, Novi, MI, USA, 8Mount Sinai Hospital,
New York, NY, USA, 9US Oncology Research, Columbia, MD, USA, 10Mayo Clinic, Jacksonville, FL, USA, 11Celgene Corporation,

Summit, NJ, USA, 12Wake Forest School of Medicine, Winston-Salem, NC, USA

Background: There are limited real-world data on effects of initial treatment in newly-diagnosed multiple myeloma(NDMM). This analysis assessed the role of initial treatment on HRQoL and outcomes in NDMM without intent for
immediate transplant, comparing some EU standard regimens vs a US standard of care (lenalidomide-bortezomibdexamethasone; RVd) using data from the Connect MM Registry.
Methods: HRQoL questionnaires and clinical assessments were conducted at baseline and quarterly until death or
discontinuation. Changes in HRQoL assessments during quarters 1-4 of initial treatment and survival outcomes, adjusted
for covariates via propensity score, were examined for RVd vs VMP (bortezomib-melphalan-prednisone) and RVd vs Vd
or VMP. Patients were censored by data cut-off (1/15/2018), 1-year follow-up, transition off initial treatment, progressive
disease, or study discontinuation.
Results: Baseline characteristics and HRQoL assessment completion rates were generally similar among groups(n=1037; eg EQ-5D at Q4: 67%-80%). There were significantly higher HRQoL improvements with RVd vs Vd or VMP
for myeloma symptoms (FACT-MM subscale), utilities (EQ-5D), and pain (BPI; P<0.05). Adjusted PFS and OS weresignificantly longer with RVd (vs Vd or VMP: 27.3 vs 19.4 months [P=0.0003] and 60.0 vs 44.4 months [P=0.0027],
respectively).

77

プレナリー２Conclusions: In this analysis of the largest US MM registry, initial treatment with RVd shows no deterioration in
HRQoL vs VMP or Vd, regimens commonly used in the EU, and significant improvements in survival. These findings
provide meaningful real-world evidence on the effects of treatment choice among patients with NDMM without intent
for immediate transplant.

プレナリー（Plenary）

PL2-4

新規薬剤時代における 65 歳以上骨髄腫の自家造血幹細胞移植の安全性と有効性：JSHCT
MM WG study
Efficacy and safety of autologous stem cell transplantation in elderly patients with multiple
myeloma in the era of novel agents: JSHCT MM WG study

水野 昌平 1、河村 浩二 2、花村 一朗 1、角南 一貴 3、森
中澤 英之 7、牧田 雅典 3、賀古 真一 2、澤 正史 8、上田
熱田 由子 12,13、高松 博幸 14、高見 昭良 1

毅彦 4、中村
恭典 9、髙橋

文彦 5、飯田 真介 6、寛行 10、神田 善伸 2、一戸辰夫 11、

Shohei Mizuno1, Koji Kawamura2, Ichiro Hanamura1, Kazutaka Sunami3, Takehiko Mori4, Fumihiko Nakamura5,

Shinsuke Iida6, Hideyuki Nakazawa7, Masanori Makita3, Shinichi Kako2, Masashi Sawa8, Yasunori Ueda9, Hiroyuki Takahashi10,
Yoshinobu Kanda2, Tatsuo Ichinohe11, Yoshiko Atsuta12,13, Hiroyuki Takamatsu14, Akiyoshi Takami1
1

愛知医科大学 血液内科、2自治医科大学付属さいたま医療センター 血液科、3岡山医療センター 血液内科、
慶應義塾大学医学部 血液内科、5国立国際医療研究センター 血液内科、6名古屋市立大学病院 血液・腫瘍内科、
7
信州大学医学部附属病院 血液内科、8安城更生病院 血液・腫瘍内科、9倉敷中央病院 血液内科、10横浜市立大学
附属病院 血液内科、11広島大学原爆放射線医科学研究所 血液・腫瘍内科、12日本造血細胞移植データセンター、
13
名古屋大学大学院医学系研究科 医療行政学、14金沢大学 医薬保健研究域医学系血液・呼吸器内科
4Division of Hematology, Department of Internal Medicine, Aichi Medical University, Japan, 2Division of Hematology, Saitama

1

Medical Center, Jichi Medical University, Japan, 3Department of Hematology, National Hospital Organization Okayama Medical

Center, Japan, 4Division of Hematology, Department of Medicine, Keio University School of Medicine, Japan, 5Division of

Hematology, National Center for Global Health and Medicine, Japan, 6Department of Hematology and Oncology, Nagoya City
University Hospital, Japan, 7Division of Hematology, Department of Internal Medicine, Shinshu University School of Medicine,Japan, 8Department of Hematology and Oncology, Anjo Kosei Hospital, Japan, 9Department of Hematology/Oncology

and Transfusion and Hemapheresis Center, Kurashiki Central Hospital, Japan, 10Department of Hematology and Clinical

Immunology, Yokohama City University Hospital, Japan, 11Department of Hematology and Oncology, Research Institute for

Radiation Biology and Medicine, Hiroshima University, Japan, 12Japanese Data Center for Hematopoietic Cell Transplantation,

Japan, 13Department of Healthcare Administration, Nagoya University Graduate School of Medicine, Japan, 14Department of

Hematology/Respiratory Medicine, Faculty of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa
University, Japan

Introduction: We examined safety and efficacy of auto-HCT for multiple myeloma among patients with 65 years ofage or older. Patients: We analyzed 2056 patients with 16 years of age or older who underwent auto-HCT for multiple
myeloma in 2007 and 2014. Patients were selected according to the following criteria: 1) first auto-HCT with peripheral
blood stem cell; 2) the condition regimen: MEL alone; 3) exclusion of the planned tandem transplantation. A total of2056 patients fulfilled these selection criteria, and 287 were 65 years of age or older. Results: The median age at thetransplantation was 66 years old in the elderly group and 57 years old in the younger group. We performed a matchedpair analysis based on the propensity score and, 263 patients were extracted from each of the two groups. The probabilityof 100-day TRM was 0.4% in the younger group and 1.2% in the elderly group with no significant difference (p=0.315)
in a propensity score matched pair analysis. OS at five years after transplantation was 62.5% in the younger group and63.5% in the elderly group with no significant difference (p=0.561). In multivariate analysis, gender, immunoglobulin
subtype, ISS stage, unfavorable cytogenetic abnormalities, disease status, and PS were significantly associated with OS,
but age was not associated. Conclusion: OS and 100-day TRM were not significantly different in younger and elderlygroups who underwent auto-HCT with multiple myeloma. We showed that auto-HCT is safe and efficacious for elderly
patients with multiple myeloma, particularly in the era of novel agents.

78プレナリー（Plenary）

PL2-5
小林
末永

宏紀、寺尾
孝生

多発性骨髄腫患者における腎機能回復の予測因子
The predictive factor of renal recovery in the patients with multiple myeloma
俊紀、津島

隆史、安部

佳亮、三浦

大典、成田

健太郎、北舘明宏、竹内正美、

Hiroki Kobayashi, Toshiki Terao, Takafumi Tsushima, Yoshiaki Abe, Daisuke Miura, Kentaro Narita, Akihiro Kitadate,
Masami Takeuchi, Kosei Matsue

亀田総合病院 血液腫瘍内科

Department of Hematology and Oncology, Kameda Medical Center, Japan

Renal impairment (RI) is one of the most common complication of multiple myeloma (MM), and major cause ofmorbidity and mortality in patients with MM. We retrospectively analyzed the clinical variables that affect renal recoveryof patients with RI in the current era. Maximal renal response was evaluated according to IWMG renal response criteria.
Major renal response was defined as achieving PRrenal and CRrenal. The initial study population consisted of 241
consecutive patients with newly diagnosed MM (NDMM) between January 2008 and November 2018 at our institute.
Moderate to severe RI (eGFR<50mL/min/1.73m2) was identified 108 patients (44.8%). The percentage of the patientswith light-chain only isotype was 27.8%, and 58.3% of the patients had kappa light chain. According to IMWG renal
response criteria, 51.8% of the patients achieved major renal response, including PRrenal 4.6%, CRrenal 47.2%. There
were significant differences in age, calcium and the level of erythropoietin between the patients with or without major
renal response, although reduction of FLC and light chain only isotype was not statistically significant. Erythropoietin≥25mIU/ml was associated with shorter time to major renal response (P <0.001). On multivariate analysis, erythropoietin≥25mIU/ml remained as the independent predictor for major renal response (P <0.001). Our results indicate that the levelof erythropoietin could show positive predictive factor for renal recovery in the patients with renal impairment in the eraof novel agents.

プレナリー２79

ポスター発表（Poster Presentation）

ポスター発表（Poster Presentation）

P1-1

正常 B リンパ球由来 iPS 細胞を用いた多発性骨髄腫の発生機序の解明に向けて
Attempt to elucidate the mechanism of development of multiple myeloma using iPS cells
derived from normal B cells

坂井 晃 1、柳 亜希 1、津山 尚宏 1、菅井 美咲 1、阿部 悠 1、柳井 祐佳理 1、太田 明伸 2、Karnan Sivasundaram2、重村 倫成 3、笹谷 めぐみ 4、神谷 研二 4、花村 一朗 2、池添 隆之 5、小野寺

雅史 6

Akira Sakai , Aki Yangi , Naohiro Tsuyama , Misaki Sugai , Yu Abe , Yukari Yanai , Akinobu Ota , Karnan Sivasundaram2,
1

1

1

1

1

1

2

Tomonari Shigemura3, Megumi Sasatani4, Kenji Kamiya4, Ichiro Hanamura2, Takayuki Ikezoe5, Masafumi Onodera61

福島県立医科大学医学部 放射線生命科学講座、2愛知医科大学 血液内科学講座、
3
信州大学医学部 小児科学講座、4広島大学 原医研 分子発がん制御、5福島県立医科大学医学部 血液内科学講座、
6
国立成育医療研究センター 成育遺伝研究部

Dept. of Radiation Life Sciences, Fukushima Medical University School of Medicine, Japan, 2Dept. of Hematology, Aichi Medical

1

University School of Medicine, Japan, 3Dept. of Pediatrics, Shinshu University School of Medicine, Japan, 4Dept. of Experimental

Oncology, RIRBM, Hiroshima University, Japan, 5Dept. of Hematology, Fukushima Medical University School of Medicine, Japan,
Dept. of Genetics, National Research Institute for Child Health and Development, Japan

6

Cells of origin of multiple myeloma (MM) have not ben identified. On the other hand, myeloma cells are derived
from mature B cells based on immunoglobulin H (IgH) gene analysis. Chromosomal aberrations such as trisomy andchromosomal translocation play a critical role in early tumorigenesis of MM. We hypothesize that the reprograming of
mature B cells, in which IgH gene rearrangements have mainteined, are the origin of MM. We suggest that mature B cells
gain a potential by reprograming, and then chromosomal aberrations cause the onset of abnormal B cells as a myelomainitiating cells during B cell redifferentiation. To elucidate the myeloma-initiating cells, we established normal B cellderived induced pluripotent stem cells (BiPSCs; BiPSC13 and MIB2-6). These BiPSCs maintain VDJ rearrangementof the IgH gene, and they can be induced by the tet-off system to express activation-induced cytidine deaminase (AID;
BiPSC13-AID and MIB2-6-AID) and differentiate into hematopoietic progenitor cells (HPCs) (Scientific Rep, 2017). We
then introduced chromosomal translocation t(11;14) and p53 deletion into BiPSCs to develop abnormal B cells.

82ポスター発表（Poster Presentation）㊝ P1-2池田

翔 1、阿部

Hexokinase-2(HK2) は低酸素誘導性オートファジーを制御し骨髄腫細胞のプロテアソーム阻
害薬耐性に寄与する
Hexokinase-2 (HK2) regulates hypoxia-induced autophagy, leading to resistance ofproteasome inhibitor of multiple myeloma
史人 1、北舘明宏 1,2、小林敬宏 1、髙橋

直人 1、田川博之 1

Sho Ikeda1, Fumito Abe1, Akihiro Kitadate1,2, Takahiro Kobayashi1, Naoto Takahashi1, Hiroyuki Tagawa1
1

秋田大学医学部 血液・腎臓・膠原病内科、2亀田総合病院 血液・腫瘍内科

Department of Hematology, Nephrology, and Rheumatology, Akita University, Japan, 2Department of Hematology and1

Oncology, Kameda General Hospital, Japan(Background) Autophagy is an intracellular process that encapsulates cytoplasmic components, which are directed to
the lysosome for degradation. Autophagy and proteasome prevent cell death that is caused by excessive endoplasmic
reticulum (ER) stress in myeloma cells. Although proteasome inhibitors (PIs) are key drug for multiple myeloma (MM),they induce treatment resistance. This might be because reciprocal autophagy could be induced in MM cells of the bonemarrow microenvironment (BMM), which is under hypoxia. Because it has been known that hypoxia inducible glycolytic
enzyme, HK2 can induce autophagy, its upregulation in BMM may contribute to the treatment resistance of MM.
(Aim and methods) To clarify the association of HK2, autophagy, and hypoxic stress in myeloma cells, and to obtainrational basis for a novel therapeutic strategy against MM, we performed following experiments.
(Results) In hypoxic condition, we found that HK2 knockdown and its inhibitor (3-bromopyruvate) induced apoptosis,
leading to increase the effect of PIs. In hypoxia, we observed p62 downregulation and TC3-II upregulation, known as
autophagy-related proteins, in accompanied with enhanced autophagosomes and lysosomes (electron microscopic).
However, HK2-knockdown/inhibitor inhibited these inductions, demonstrating that HK2-inhibition inhibits hypoxiainducible autophagy.
(Conclusion) Our results suggested that protection from ER stress might be mainly due to HK2-inducible autophagy in
MM microenvironment. Therefore, combination use of PIs and HK2 inhibitor could be a new approach for resistant MM.

ポスター１

83

ポスター発表（Poster Presentation）

P1-3

多発性骨髄腫の微小環境は可溶型 SLAMF7 以外の要因によって樹状細胞において Th1 誘導を抑制し Th2 誘導を増強する
Myeloma cells have the ability to suppress Th1-inducing capacity but enhance Th2mediated response of DCs by factors other than soluble SLAMF7

東 由子、伊藤 量基、重坂 実、今井 開、斎藤 陵、小西 晶子、吉村佐竹 敦、中谷 綾、宮地 理彦、石井 一慶、野村 昌作

英晃、堀田

雅章、中西

孝尚、藤田

真也、

Yoshiko Azuma, Tomoki Ito, Minoru Shigesaka, Kai Imai, Ryo Saitou, Akiko Konishi, Hideaki Yoshimura, Masaaki Hotta,
takahisa Nakanishi, Shinnya Hujita, Atushi Satake, Aya Nakaya, Toshihiko Miyadi, Kazuyoshi Ishii, Shosaku Nomura

関西医科大学第一内科学講座

1st. Department of Internal Medicine, KMU, Japan

Since myeloma cells together with immune cells are immersed in the pathogenic micro-environment, understanding
the influence of microenvironment against myeloma cells may lead to the development of treatment for MM. We
focused on the effects of myeloma environment to modulate the human myeloid dendritic cells (mDCs), which are themajor regulators to induce Th1 or Th2 responses. To evaluate the functions of soluble factors/components derived frommyeloma cells, we analyzed whether supernatants of MM cell lines could modulate mDC functions. We here found thatsupernatants of MM cell lines did not affect mDC survival and their CD86 expression. Of note, the supernatants inhibited
mDC-derived IL-12 production in response to TLR-ligand(R848), while in response to Th2-inducing cytokine TSLP,
dose-dependently enhanced the Th2-recruiting chemokine CCL17/TARC production, which functions as chemoattractant
for memory Th2 cells and promotes humoral response. Thus, MM microenvironment could have the potential to shift
DCmediated response from Th1 to Th2. To clarify whether sSLAMF7 in the supernatant of MM cell lines play a role in
the Th1/Th2 modulating effect, we calculated the sSLAMF7
concentration in the supernatants cultured by FBS. However, sSLAMF7 could not be detected at all in the supernatantsof MM cell lines. Hence, factors other than sSLAMF7 from myeloma cells can trigger DCs to suppress Th1 response andto promote Th2 response. Our data suggest that the MM micro-environment, while suppress the Th1-inducing capacity,rather lead to enhance Th2 response at DC phase.

84

ポスター発表（Poster Presentation）

P1-4
上田

多発性骨髄腫において NOTCH1 と JAG1 の相互作用が増悪化を誘導する
The interaction of NOTCH1 with JAG1 induces aggressive myeloma behavior

圭馬 1、石橋真理子 2、今井

陽一 3、猪口孝一 4、田村秀人 4

Keima Ueda , Mariko Ishibashi , Yoichi Imai , Koiti Inokuchi , Hideto Tamura4
1

2

3

4

1

日本医科大学医学部 5学年、2日本医科大学微生物学・免疫学、3東京大学医科学研究所附属病院血液腫瘍内科、
4
日本医科大学血液内科

Fifth grade, Nippon Medical School, Japan, 2Department of Microbiology and Immunology, Nippon Medical School, Japan,

1

Department of Hematology and Oncology, IMSUT Hospital, The Institute of Medical Science, The University of Tokyo, Japan,

3

Department of Hematology, Nippon Medical School, Japan

4

Introduction: The NOTCH signaling pathway plays a crucial role in tumor pathogenesis. In this study, we examinedthe expression of NOTCH and its ligands in multiple myeloma (MM) and the functions of NOTCH signaling in MM
progression.
Methods and Results: The expression of NOTCH1–4 receptors and their ligands (JAG1 and -2 and DLL1, -3, -4) was
analyzed using real-time PCR and flow cytometry (FCM) in 17 MM cell lines and plasma cells obtained from MM
patients. NOTCH1, NOTCH2, and JAG1 were highly expressed in MM cell lines and primary MM cells. Next, the cellproliferation and drug sensitivity of MM cells were examined by FCM. The proliferative potential and percentage ofanti-MM agent-induced apoptotic cells blocked with anti-NOTCH1 antibody were lower and higher than with controls or
anti-NOTCH2 antibody, respectively. Furthermore, NOTCH1+ cells showed enhanced proliferation and decreased drug
susceptibility compared with NOTCH1– cells. Aggressive MM behavior in NOTCH1+ cells was suppressed by anti-JAG1
antibody. The gene expression of p21 and cyclin D1/2 in NOTCH1+ cells was upregulated, while that of apoptotic genes
was decreased.
Conclusions: This study demonstrated that NOTCH1/2 and JAG1 are highly expressed in MM and the NOTCH1–JAG1
signaling pathway induces a high malignant potential in MM. Further studies are in progress to clarify the association of
NOTCH1–JAG1 signaling with MM progression.

ポスター１

85

ポスター発表（Poster Presentation）

P1-5

血清 KL-6 値は多発性骨髄腫の予後予測因子となりうる
KL-6 may be an excellent predictor of prognosis in multiple myeloma

砂川 実香 1、石橋
今井 陽一 5、田中真理子 2、海渡 裕太 1、木下 量介 1、朝山 敏夫 1、守屋 慶一 1、半田 寛 3、佐々木 純 4、
紀奈 6、伊藤 薫樹 7、田野崎 栄 8、田中 淳司 6、小松 則夫 4、猪口 孝一 1、田村 秀人 1

Mika Sunakawa1, Mariko Ishibashi2, Yuta Kaito1, Ryosuke Kinoshita1, Toshio Asayama1, Keiichi Moriya1, Hiroshi Handa3,

Makoto Sasaki4, Yoichi Imai5, Norina Tanaka6, Shigeki Ito7, Sakae Tanosaki8, Junji Tanaka6, Norio Komatsu4, Koiti Inokuchi1,
Hideto Tamura1

1

日本医科大学 血液内科、2日本医科大学 微生物学・免疫学、3群馬大学医学部附属病院 血液内科、
4
順天堂大学医学部順天堂医院 血液内科、5東京大学医科学研究所、6東京女子医科大学 血液内科、
7
岩手医科大学 臨床腫瘍学講座、8同愛記念病院 血液内科

Division of Hematology, Nippon Medical School, Japan, 2Department of Microbiology and Immunology, Nippon Medical

1

School, Japan, 3Department of Medicine and Clinical Science, Gunma University Graduate School of Medicine, Japan, 4Divisionof Hematology, Department of Internal Medicine, Juntendo University School of Medicine, Japan, 5Department of Hematology/

Oncology, The Institute of Medical Science, The University of Tokyo, Japan, 6Department of Hematology, Tokyo Women’s

Medical University, Japan, 7Department of Medical Oncology, Iwate Medical University School of Medicine, Japan, 8Department

of Hematology, Fraternity Memorial Hospital, Japan

Introduction: KL-6, a sialylated carbohydrate glycoprotein present in human MUC1 mucin, is a known marker ofinterstitial pneumonia. MUC1 may contribute to disease progression in multiple myeloma (MM) through the β-catenin
pathway. It was reported that some MM patients with high levels of KL-6 had an aggressive clinical course. However,the clinical role and mechanism of KL-6 in MM remain unclear. We investigated the relationship between serum KL-6
levels and clinical characteristics and analyzed the function of KL-6/MUC1 in MM.
Methods and Results: We examined the difference in clinical characteristics between newly diagnosed MM patientswith high levels of KL-6 (defined as >500
U/ml, n=22) and those with normal levels (≤500 U/ml, n=173). MM patients in the high group were older and had lower
hemoglobin and higher LDH levels than those in the normal group. They had also significantly shorter progression-freesurvival time (20.2 vs 44.9 months, p<0.01). Moreover, the rate of very good partial response or better was significantly
lower in the high group. To analyze the function of KL-6, we established a KL-6-producing cell line from peripheralmononuclear cells of a refractory MM patient with elevated KL-6. Those cells expressed high MUC1 mRNA and MUC1
protein levels.
Conclusion: Serum KL-6 levels may be useful to predict prognosis in MM patients and be related to MUC1 expression.
Its production may be associated with the bone marrow microenvironment. Further studies are in progress to clarify thefunctions of KL-6/MUC1.

86

ポスター発表（Poster Presentation）㊝ P2-1
戸田

侑紀、中山

多発性骨髄腫細胞における低酸素適応のための exosome 分泌過多
Increased exosome secretion is a way of hypoxic adaptation in multiple myeloma cells
紗矢香、細木誠之、芦原英司

Yuki Toda, Sayaka Nakayama, Shigekuni Hosogi, Eishi Ashihara

京都薬科大学薬学部 病態生理学分野

Dept. Clinical & Translational Physiology, Kyoto Pharmaceutical Univ., Japan

Cancer stem cells (CSCs) of the highly tumorigenic cell population are critically associated with the poor prognosisof patients in various types of cancer. In our previous study, the multiple myeloma (MM) cells which were chronicallycultured in a hypoxic condition (1%O2) exhibited stem cell characteristics (Nakagawa Y, Ashihara E, et al. Biochem
Biophys Res Commun, 496:490-496, 2018). It suggests that MM stem cells are capable of adapting to hypoxic stressalthough the adaptation mechanism remains unclear. We focused on the excessive secretion of exosomes from hypoxiaadapted MM cells (HA-MM cells).
GW4869, an inhibitor of exosome biogenesis, increased dead cells in HA-MM cells, but not in parental cells cultured ina normoxic condition (20%O2). With the addition of HA-MM-derived exosomes, GW4869-induced cell death was notattenuated. It indicates that HA-MM cells are likely to release exosomes to maintain the intracellular environment in astate of homeostasis, but not to receive them for autocrine signal.
Under a hypoxic condition, cancer cells promote lactate production via upregulation of glycolysis-related molecules.
GW4869 diminished the upregulated hexokinase 2 expression and decreased intracellular lactate amounts. Thus, thefailure of exosome secretion might cause metabolic catastrophe toward cell death.
In conclusion, enhancement of exosome secretion is a survival strategy for hypoxic adaptation in MM stem cells. This
study could provide a critical insight to develop a novel strategy for CSC-targeted therapy.

ポスター１
ポスター２

87

ポスター発表（Poster Presentation）

P2-2

不動は骨吸収と骨髄腫進展を促進させる
Immobilization promotes bone resorption and tumor expansion in myeloma

谷本 幸多朗 1,2、日浅 雅博 1,2、天真 寛文 1,2、寺町 順平 2,3、Mohannad Ashtar1,2、小田 明日香 2、岩佐 昌美 2、
曾我部 公子 2、大浦 雅弘 2、原田 武志 2、中村 信元 2、三木 浩和 5、遠藤 逸朗 4、田中 栄二 1、松本 俊夫 6、
安倍 正博 2
Kotaro Tanimoto1,2, Masahiro Hiasa1,2, Hirofumi Tenshin1,2, Jumpei Teramachi2,3, Ashtar Mohannad1,2, Asuka Oda2,

Masami Iwasa2, Kimiko Sogabe2, Masahiro Oura2, Takeshi Harada2, Shingen Nakamura2, Hirokazu Miki5, Itsuro Endo4,
Eiji Tanaka1, Toshio Matsumoto6, Masahiro Abe2

1

徳島大学大学院 医歯薬学研究部 口腔顎顔面矯正学分野、
徳島大学大学院 医歯薬学研究部 血液・内分泌代謝内科学分野、
3
徳島大学大学院 医歯薬学研究部 組織再生制御学、4徳島大学大学院 医歯薬学研究部 生体機能解析学分野、
5
徳島大学病院 輸血・細胞治療部、6徳島大学 藤井節郎記念医科学センター
2

Department of Orthodontics and Dentofacial Orthopedics, University of Tokushima, Tokushima, Japan, 2Department of

1

Hematology, Endocrinology and Metabolism, University of Tokushima, Tokushima, Japan, 3Department of Histology and Oral

Histology, University of Tokushima, Tokushima, Japan, 4Department of Chronomedicine, University of Tokushima, Tokushima,

Japan, 5Division of Transfusion Medicine and Cell Therapy, Tokushima University Hospital, Tokushima, Japan, 6Fujii Memorial
Institute of Medical Sciences, University of Tokushima, Tokushima, Japan

Patients with myeloma (MM) often suffer from immobilization by bone fractures. In the present study, we explored theimpacts of immobilization or mechanical unloading on MM tumor expansion. Right hind legs of mice were unilaterally
immobilized by sciatic denervation or casting with adhesive bandage. MicroCT revealed substantial volume reduction of
not only muscle but also trabecular bone in the immobilized legs. Morphological analysis revealed increase in osteoclast
numbers and activity without apparently affecting bone formation in the immobilized legs. We then inoculated luciferasetransfected mouse 5TGM1 MM cells into tibiae in the immobilized hind legs in mice with the denervation or in intact
ones in control mice. 5TGM1 tumor expanded more rapidly in the tibiae in mice with the denervation than control miceas shown by in vivo imaging and serum levels of MM cell-derived IgG2b. The acceleration of MM tumor growth byimmobilization was further confirmed by simultaneous MM cell inoculation into tibiae in the immobilized (right) or
intact (left) hind legs in the same mice. MM tumor growth was more accelerated by the immobilized legs in mice treatedwith the denervation as well as casting. The acceleration of MM tumor growth by immobilization was suppressed by theanti-resorptive agent zoledronic acid. These results demonstrate that immobilization aggravates bone destruction andMM tumor expansion. Given RANK ligand induction by osteocytes under mechanical unloading, further study on therole of osteocytes is warranted.

88ポスター発表（Poster Presentation）

P2-3
菊池

骨髄腫細胞間相互作用による薬剤耐性獲得機構の解明
The role of myeloma cell homophilic interaction in drug resistance次郎 1、長田直希 1、小山大輔 1、黒田芳明 2、安井

寛 3、古川祐雄 1Jiro Kikuchi , Naoki Osada , Daisuke Koyama , Yoshiaki Kuroda , Hiroshi Yasui , Yusuke Furukawa1
1

1

1

1

2

3

自治医科大学分子病態治療研究センター 幹細胞制御研究部、2広島西医療センター内科、3東京大学医科学研究所

Division of Stem Cell Regulation, Center for Molecular Medicine, Jichi Medical University, Japan, 2National Hospital

1

Organization, Hiroshima-Nishi Medical Center, Japan, 3Institute of Medical Science, University of Tokyo, Japan

Cell adhesion mediated-drug resistance (CAM-DR) is a major obstacle in achieving cure in patients with multiple
myeloma (MM). We have identified the underlying mechanisms of CAM-DR via interaction between MM cells
and bone marrow microenvironment including stroma cells (Oncogene 2009, J Clin Invest 2015, Cancer Res 2018).
However, little is known about the role of MM cell homophilic interaction in CAM-DR.
In this study, we found that MM cells interacted with each other and generated cell clusters under co-culture with thestroma cell line UBE6T-7. MM cell clusters were also generated under co-culture with the other stroma cell line stromaNK, but not with fibroblasts. In addition, conditioned medium of not fibroblasts but stroma cells could generate MM cellclusters. Among MM cell lines, MM.1S and KMS12-BM could generate cell clusters. The cell cluster generation was
not inhibited by anti-MM drugs, including bortezomib, lenalidomide, melphalan, daratumumab, and elotuzumab. MM
cell clusters rendered the resistance to bortezomib among these drugs.
MM cell clusters were found in myeloma patients with extramedullary disease. The myeloma cell homophilicinteraction may confer drug resistance, which provides an explanation for poor prognosis of patients with extramedullary
disease. Antibodies counteracting MM cell homophilic interaction may increase the therapeutic index in clinical settings.

ポスター２

89

ポスター発表（Poster Presentation）㊝ P2-4

ROS の骨髄腫の骨病変と癌治療関連骨減少症の誘発における重要な役割
Critical roles of ROS in induction of bone disease and cancer treatment-induced bone loss inmyelomaMohannd Ashter1、天真 寛文 2、寺町 順平 3、日浅 雅博 2、谷本 幸多朗 1、小田 明日香 4、岩佐 昌美 4、
原田 武志 4、藤井 志朗 4、香川 久美子 4、大浦 雅博 4、曽我部 公子 4、中村 信元 4、三木 浩和 5、田中 栄二 2、
松本 俊夫 6、安倍 正博 4Mohannad Ashter1, Hirofumi Tenshin2, Jumpei Teramachi3, Masahiro Hiasa2, Kotaro Tanimoto1, Asuka Oda4, Masami Iwasa4,
Takeshi Harada4, Shirou Fuji4, Kumiko Kagawa4, Masahiro Oura4, Kimiko Sogabe4, Shingen Nakamura4, Hirokazu Miki5,

Eiji Tanaka2, Toshio Matsumoto6, Masahiro Abe4
1

徳島大学大学院 口腔科学教育部 口腔顎顔面矯正学分野、2徳島大学大学院 医歯薬学研究部 口腔顎顔面矯正学分野、
徳島大学大学院 医歯薬学研究部 組織再生制御学、4徳島大学大学院 医歯薬学研究部 血液・内分泌代謝内科学分野、
5
徳島大学病院 輸血・細胞治療部、6徳島大学 藤井節郎記念医科学センター
3

Department of Orthodontics and Dentofacial Orthopedics, Tokushima University Graduate School of Oral Sciences, Japan,

1

Department of Orthodontics and Dentofacial Orthopedics, Institute of Biomedical Sciences, Tokushima University Graduate

2

School, Japan, 3Department of Tissue Regeneration, Institute of Biomedical Sciences, Tokushima University Graduate School,

Japan, 4Department of Hematology, Endocrinology and Metabolism, Institute of Biomedical Sciences, Tokushima University
Graduate School, Japan, 5Division of Transfusion Medicine and Cell Therapy, Tokushima University Hospital, Japan, 6Fujii
Memorial Institute of Medical Sciences, Tokushima University, Japan

Besides skeletal-related events by myeloma (MM), cancer treatment-induced bone loss (CTIBL) deteriorates QoL in MM
patients, posing high unmet needs. Because ROS has been demonstrated to mediate osteoclastogenesis, in the present
study we explored the role of ROS in induction of MM bone disease and CTIBL. RANKL induced ROS production in
RAW264.7 preosteoclastic cells and bone marrow-derived macrophages (BMMs); however, treatment with the xanthineoxidase inhibitor febuxostat as well as N-acetylcysteine (NAC) suppressed their ROS production and osteoclastogenesis
by RANKL. Febuxostat also alleviated osteoclastogenesis enhanced in cocultures of mouse bone marrow cells with
5TGM1 MM cells. Interestingly, doxorubicin (Dox) triggered ROS generation in RAW264.7 cells and BMMs andfacilitated their osteoclastogenesis by RANKL in a manner inhibitable with febuxostat, indicating aggravation of
osteoclastogenesis in MM through ROS induction by Dox. Moreover, febuxostat was able to stimulate osteoblastogenesis
by MC3T3-E1 preosteoblastic cells. These results collectively demonstrate that intracellular ROS plays a critical role in
RANKL- and Dox-induced osteoclastic bone resorption, and suggest that excessive ROS production disadvantageously
impacts bone resorption and formation, leading to CTIBL. Because kockdown of xanthine oxidase gene by shRNA only
partially suppressed ROS production in RAW264.7 cells by RANKL as well as Dox, further study is warranted to look
into the role of mitochondrial ROS and the regulation of bone health by the cellular redox status.

90ポスター発表（Poster Presentation）

P2-5

多発性骨髄腫細胞サブセットに対する腫瘍免疫の応答予測
Response prediction and mechanisms of tumor immunosurveillance against multiple
myeloma cellsubsets

八幡 真人 1,2、Siti Sarah Daud1、Ryo Takahashi1、Ankurina Sharma1、Sathish Gopalakrishnan3、Kiat Hoe Ong4、八幡 信代 5、Wee Joo Chng6
Makoto Yawata1,2, Siti Sarah Daud1, Ryo Takahashi1, Ankurina Sharma1, Sathish Gopalakrishnan3, Kiat Hoe Ong4,

Nobuyo Yawata5, Wee Joo Chng6
1

Department of Pediatrics, National University of Singapore and National University Health System, Singapore, 2Singapore

Institute for Clinical Sciences, Agency for Science Technology and Research, Singapore, 3Department of Haematology,

Singapore General Hospital, Singapore, 4Department of Haematology, Tan Tock Seng Hospital, Singapore, 5Department ofOphthalmology, Kyushu University, Japan, 6Department of Haematology-Oncology, National University of Singapore andNational University Health System, Singapore

There exist multiple cellular subsets of tumor cells within a myeloma patient and the frequencies of these subsets
fluctuate over the course of disease and therapy. These cellular subsets evolve under constant exposure to tumor
immunosurveillance. In this study, we aimed to understand the mechanisms of tumor escape from NK cell responses andto profile the immunogenicity of myeloma subsets in clinical specimens.
We used high-dimensional flow cytometry on bone marrow aspirates to distinguish myeloma
subsets and subsequently to sort them individually (4 laser cell sorter, iCyt).
Antibodies used were anti-CD138, -CD38, -CD20, -CD19, -CD319, -CD27, -CD45, -CD3, -CD56, -CD14, -NKp80 -cyKappa-Ig, -cy-Lambda-Ig. RNA was extracted from the sorted cells and transcriptome profiling was conducted using theAgilent Sure Print G3 8x60 human microarray system.
We identified five myeloma subsets that were present relatively often in the specimens however the abundance of thesubsets differed substantially by patient. Expression profiles of genes encoding ligands for activating and inhibitory
immune cell receptors indicated that the main mechanism of immune escape from NK cell-mediated responses formyeloma subsets that have a more malignant phenotype is by simultaneously downregulating specific activating
pathways while increasing inhibitory signaling. Because the NK cell repertoires differ substantially by human individual,such immunological profiling and response prediction will be useful in prognostication as myeloma subpopulations
become characterized in detail.

ポスター２

91

ポスター発表（Poster Presentation）

P3-1

多発性骨髄腫 MRD 検出における SRL 8 カラー・1 チューブ MFC と EuroFlow-NGF の比較
Comparison of MRD detection in multiple myeloma between SRL 8-color single-tube and
EuroFlow 8-color 2-tube multiparameter flow cytometry methods

高松 博幸 1、鎧高
中尾 眞二 1、末永

健志 1、藤澤孝生 4

桃子 1、小堀一弥 2、塙

正子 2、山下剛史 3、村田了一 3、上田幹夫 3、

Hiroyuki Takamatsu1, Takeshi Yoroidaka1, Momoko Fujisawa1, Kazuya Kobori2, Masako Hanawa2, Takeshi Yamashita3,

Ryoichi Murata3, Mikio Ueda3, Shinji Nakao1, Kosei Matsue4
1

金沢大学 血液・呼吸器内科、2株式会社エスアールエル、3恵寿金沢病院 内科、4亀田総合病院 血液・腫瘍内科

Hematology/Respiratory Medicine, Kanazawa University, Japan, 2SRL, Inc., Japan, 3Division of Internal Medicine, Keiju Kanazawa

1

Hospital, Japan, 4Department of Hematology/Oncology, Kameda Medical Center, JapanWe developed a new single-tube, inexpensive (<200 USD/sample as of January of 2019) 8-color multiparameter flow
cytometry (MFC) method (SRL-Flow) based on the EuroFlow-next generation flow (NGF) (tube 2 only) to assess
the minimal residual disease (MRD) negative status that is believed to be a milestone in curing patients with multiple
myeloma (MM). In the present study, we used 45 bone marrow samples from patients with MM, including 11 anti-CD38
monoclonal antibody (10 daratumumab and 1 isatuximab)-treated cases. The sample preparation protocol of SRL-Flowwas identical to that of EuroFlow-NGF, and the antibody panel of SRL-Flow, 8-color, 1-tube was as follows: CD138V450/
CD27V500/CD38ME (multiepitope)FITC /CD56PE/CD45PerCP-Cy5.5/CD19PE-Cy7/cytoplasmic (Cy) Immunoglobulin (Ig) κAPC/
CyIgλAPC-H7. To identify abnormal plasma cells (aPCs) of patients with MM who received anti-CD38 monoclonal
antibody, we used an anti-CD45 and anti-CD138 antibodies (Abs) panel instead of an anti-CD45 and anti-CD38 Abs
panel. We comparatively analyzed the total nucleated cell numbers, total PC ratios, and abnormal plasma cell (MRD)
ratios between the SRL-Flow and EuroFlow-NGF. High correlations (r > 0.9) in total PC and MRD ratios were notedamong SRL-Flow, original EuroFlow-NGF (2 tubes), and EuroFlow-NGF (tube 2 only), suggesting that SRL-Flow is an
inexpensive alternative MFC method to EuroFlow-NGF (<350 USD/sample) to assess MRD in MM.

92

ポスター発表（Poster Presentation）

P3-2

VS38 はダラツムマブ使用下でも CD38 に代わり形質細胞を検出し得る有用な抗体である
VS38 as a promising CD38 substitute antibody for flow cytometric detection of plasma cells
in the daratumumab era

河田 岳人 1,2、水田 駿平 3,4、川畑
為金 現 1、渡邊 光正 1

宏志 3、山根範子 3、物延

沙耶 3、駒井隆夫 3、木場悠介 1、右京

直哉 1、Takahito Kawata1,2, Shumpei Mizuta3,4, Hiroshi Kawabata3, Noriko Yamane3, Saya Mononobe3, Takao Komai3, Yusuke Koba1,
Naoya Ukyo1, Akira Tamekane1, Mitsumasa Watanabe1

1

兵庫県立尼崎総合医療センター 血液内科、2京都大学大学院医学研究科 血液・腫瘍内科学、3
兵庫県立尼崎総合医療センター 検査部、4神戸大学大学院保健学研究科 病態解析学領域

Department of Hematology, Hyogo Prefectural Amagasaki General Medical Center, Japan, 2Department of Hematology and1

Oncology, Graduate School of Medicine, Kyoto University, Kyoto, Japan, 3Department of Cliniacal Laboratory, Hyogo Prefectural
Amagasaki General Medical Center, Japan, 4Laboratory of Hematology, Division of Medical Biophysics, Kobe University

Graduate School of Health Sciences, Hyogo, Japan

Development of effective therapies has enabled long-term survival for many patients with multiple myeloma (MM).
However, antibody drug administration, such as daratumumab that binds to plasma cell (PC) surface proteins, would
prevent PC detection by flow cytometry. We proposed VS38 as an alternative antibody for anti-CD38. VS38 recognizes
cytoskeleton-linking membrane protein 63 (CLIMP-63) on the rough endoplasmic reticulum, and it is suggested that
CLIMP-63 proteins are expressed in secretory cells. We investigated VS38 staining in normal hematopoietic cells fromfive controls, followed by PCs from 20 cases of plasma cell disorder (PCD). In normal hematopoietic cells, although
VS38 stained monocytes, myeloid cells, and part of B-cells, PCs were significantly and brightly stained by VS38.
There was no significant difference in VS38 staining between normal and abnormal PCs obtained from five cases ofmonoclonal gammopathy of undetermined significance. Furthermore, PCs in 20 PCD cases were clearly identified by
VS38 in all cases, in contrast to CD38, even in daratumumab-administered patients whose CD38 epitopes on PCs weremasked. These results suggest that VS38 as a flow cytometry antibody can contribute to PC detection, independent oftherapeutic treatment.

ポスター３

93

ポスター発表（Poster Presentation）

P3-3
坂本 淳 1、石田
阿部 有 2、吉識鈴木 憲史 2

10color-MFC の基礎検討
Basic study of Multiparameter flow cytometry
禎夫 2、野間 芳弘 1、金子 成人 1、前田 亜希 1、浜崎 博行 1、塚田 信弘 2、岡塚由実子 2、宮崎 寛至 2、佐藤 広太 2、小倉 瑞生 2、宇藤 唯 2、余語 孝夫 2、梨本

貴世志 2、
淳一郎 2、

Jun Sakamoto1, Tadao Ishida2, Yoshihiro Noma1, Shigeto Kaneko1, Aki Maeda1, Hiroyuki Hamazaki1, Nobuhiro Tsukada2,
Kiyoshi Okazuka2, Yu Abe2, Yumiko Yoshiki2, Kanji Miyazaki2, Kota Sato2, Mizuki Ogura2, Yui Uto2, Takao Yogo2,

Junichiro Nashimoto2, Kenshi Suzuki2
1

株式会社ビー・エム・エル 細胞性免疫課、2日本赤十字社医療センター 血液内科

BML, Inc, Japan, 2Department of Hematology, Japanese Red Cross Medical Center, Japan

1【Background】
The progress in new drug development has improved the outcome from the treatment of multiple myeloma(MM).
We have evaluated using the multi-parameter flow cytometry (MFC) where highly sensitive detection is desired for
determination of treatment effect for Minimal Residual Disease (MRD). Although EuroFlow MM-MRD is a global
standard for MRD detection by MFC, the application is limited to research use only due to the Japanese health insurance
reimbursement. On the other hand, if the sensitivity of 10-5 level can be achieved in 10color-MFC, clinical use may
be possible based on the international guideline of International Clinical Cytometry Society(ICCS). In this study, we
compared EuroFlow MM-MRD with 10color-MFC using MM(or other) bone marrow samples.
【Method】
Bone marrow samples from 50 patients were subject to MRD detection by EuroFlow MM-MRD and 10color-MFC. The
samples were processed and analyzed by EuroFlow MM-MRD according to EuroFlow standard operating procedure.
CD38 multi epitope, CD138, CD45, CD56, CD19, CD27, CD81, CD117, cIgκ, and cIgλ were used as antibody panel set
for 10color-MFC and processed according to the ICCS guideline.
【Results】
Preliminary results using 25 samples showed a correlation coefficient between EuroFlow MM-MRD and 10color-MFC
to be R=0.8259. Results from 50 samples will be analyzed and presented.

94ポスター発表（Poster Presentation）

P3-4
竹下

骨髄腫臨床検体バンクの構築およびクローナリティ解析についての進捗報告
Establishment of clinical myeloma specimen bank and progress report of clonality analysis

昌孝 1,2、小玉信之 2、平井理泉 1、谷村

聡 1、岡崎幸治 1、奥田優子 1、工藤大輔 1、三輪

哲義 1,2Masataka Takeshita , Nobuyuki Kodama , Risen Hirai , Akira Tanimura , Kouji Okazaki , Yuko Okuda , Daisuke Kudo1,
1,2

2

1

1

1

1

Akiyoshi Miwa1,2

1

地域医療振興協会 東京北医療センター 血液内科、2国際骨髄腫先端治療研究センター

Department of Hematology, Tokyo-Kita Medical Center, Japan, 2International Myeloma Center for Advanced Research and

1Treatment, JapanAs we reported on previous meeting of JSM, we have established a clinical specimen bank at IMC-ART(International
Myeloma Center for Advanced Research and Treatment). We are stocking bone marrow, peripheral blood and serum
samples from patients who are treated at Tokyo-Kita Medical Center.
Median age at diagnosis: 61.5(26-74)
Mononuclear cells from pre-treatment and serial post-treated bone marrow samples were separated to CD138(+)fraction
and CD138(-)fraction with MACS, then frozen or proceeded to library preparation for next generation sequence.
Genomic DNA and RNA were extracted from peripheral blood for preparation. Peripheral mononuclear cells and serums
were also stocked.
In last meeting, we reported about measurement of minimal residual disease with in-house EuroFlowTM method, but we
did not describe about clonality analysis.
In this presentation we report about clonality assay of plasma cells referring previously described BIOMED-2 guideline.
There are many unsolved questions regarding multiple myeloma, for example, pathogenesis, mechanism of diseaseprogression, relapse or acquirement of drug resistance.
Clinical features of young-onset disease or primary refractory disease imply an existence of disease accelerating factor.
Precise analysis of these samples will lead us to novel treatment target or new treatment strategy.

ポスター３

95

ポスター発表（Poster Presentation）

P3-5

NGS による AL アミロイドーシスでのクローナル免疫グロブリンλ遺伝子の同定
Identification of clonal immunoglobulin λ light-chain gene rearrangements in AL
amyloidosis by next generation sequencing

木村 賢司 1、塚本 祥吉 1、宮崎 寛至 2、真子 ( 川尻 ) 千華 3、Rahmutulla Bahityar4、福世 真樹 4、
大島 ( 長谷川 ) 渚 1、三川 紫緒 1,5、竹田 勇輔 1、三村 尚也 1,5、武内 正博 1、大和田 千桂子 1、井関松坂 恵介 4、金田 篤志 4、石田 禎夫 2、鈴木 憲史 2、中世古 知昭 6、堺田 惠美子 1

徹 1,5、Kenji Kimura1, Shokichi Tsukamoto1, Kanji Miyazaki2, Chika Kawajiri-Manako3, Rahmutulla Bahityar4, Masaki Fukuyo4,

Nagisa Oshima-Hasegawa1, Shio Mitsukawa1,5, Yusuke Takeda1, Naoya Mimura1,5, Masahiro Takeuchi1, Chikako Ohwada1,
Tohru Iseki1,5, Keisuke Matsusaka4, Atsushi Kaneda4, Tadao Ishida2, Kenshi Suzuki2, Chiaki Nakaseko6, Emiko Sakaida1
1

千葉大学医学部附属病院 血液内科、2日本赤十字医療センター 血液内科、
大網白里市立国保大網病院、4千葉大学大学院医学研究院 分子腫瘍学、5千葉大学医学部附属病院 輸血・細胞療法部、
6
国際医療福祉大学医学部 血液内科
3

Department of Hematology, Chiba University Hospital, Chiba, Japan, 2Department of Hematology, Japanese Red Cross medical

1

center, Tokyo, Japan, 3Department of Hematology, Oami Municipal Hospital, Chiba, japan, 4Department of Molecular Oncology,

Chiba University Graduate School of Medicine, Chiba, Japan, 5Department of Transfusion Medicine and Cell Therapy, Chiba

University Hospital, Chiba, Japan, 6Department of Hematology, International University of Health and Welfare, Narita, Japan

Introduction: AL amyloidosis is caused by the deposition of clonal immunoglobulin (IG) light chains (LCs, λ/κ: 3/1)
made from plasma cells in bone marrow (BM). However, there has been no study analyzing the germlines of plasma cellsby next generation sequencing (NGS) in AL amyloidosis. In this study, we aimed to identify the clonal composition of IG
λ chain variable (IGLV) genes in BM cells in patients with AL amyloidosis.
Materials and Methods: BM cells were obtained from patients with AL amyloidosis (N = 19), MGUS (N = 7), multiple
myeloma (MM, N = 6) with monoclonal λ LCs, and malignant lymphoma without BM invasion (normal control, N = 4)
in Japanese Red Cross Medical Center and Chiba University Hospital. NGS of IGLV1–3 genes in BM cells was carriedout using an Illumina MiSeq sequencer and LC repertoires were analyzed by Vidjil program.
Result: The most abundant IGLV gene accounted for no more than 1% and there was no dominant germline in normal
control samples, whereas clonal composition of IGLV genes (more than 1% of the same V-region, J-region and CDR3
sequence or existing dominant germline) were found in MM (6/6), MGUS (7/7), and AL amyloidosis (17/19). However,the size of clones were quite small: 0.5–14.6% in MGUS, 0.8–12.7% in AL amyloidosis compared to MM (12.6–29.1%).
Conclusions: We successfully identified the clonal composition of IGLV genes in BM cells in most patients with AL
amyloidosis. The size of clone was quite small and further investigation is needed to understand the relationship between
clonal IGLV genes and clinical manifestations.

96ポスター発表（Poster Presentation）

保仙

ポスター４

P4-1

多発性骨髄腫に対する新規 CAR T 細胞療法の開発
Development of a novel CAR T-cell therapy for multiple myeloma

直毅

Naoki Hosen

大阪大学大学院医学系研究科 癌幹細胞制御学

Department of Cancer Stem Cell Biology, Osaka University Graduate School of Medicine, Japan

We discovered that the active conformer of an integrin could serve as a specific therapeutic target for multiple myeloma(MM). We first identified MMG49 as an MM-specific mAb after screening more than 10,000 anti-MM mAb clones, andfound that it specifically recognized a subset of integrin b7 molecules. The MMG49 epitope is located in the N-terminal
region of the b7 chain, which is predicted to be inaccessible in the resting integrin conformer, but exposed in the active
conformation. Elevated expression and constitutive activation of integrin b7 conferred high MMG49 reactivity on MM
cells, whereas MMG49 binding was barely detectable in other types of cells, including normal integrin b7+ lymphocytes.
Furthermore, T cells transduced with MMG49-derived chimeric antigen receptor (CAR) exerted anti-MM effects
without damaging normal hematopoietic cells. These results not only demonstrate that MMG49 CAR T-cell therapy is
promising for MM, but also provide a definitive evidence that a receptor protein with a rare but physiologically relevant
conformation could serve as a target for cancer immunotherapy. I will present our preparation for a clinical trial.

ポスター３

97

ポスター発表（Poster Presentation）

P4-2
太田

骨髄腫細胞における PBZ binding kinase の腫瘍促進作用と治療標的分子としての可能性
Role of PBK in multiple myeloma cell growth: implication of PBK in novel molecular targets
for anti-myeloma therapy

明伸 1、花村一朗 2、Karnan Sivasundaram1、高見昭良 2、細川好孝 1

Akinobu Ota1, Ichiro Hanamura2, Karnan Sivasundaram1, Akiyoshi Takami2, Yoshitaka Hosokawa1
1

愛知医科大学 医学部生化学講座、2愛知医科大学 医学部血液内科学講座

Department of Biochemistry, Aichi Medical University School of Medicine, Japan, 2Division of Hematology, Department of

1

Internal Medicine, Aichi Medical University School of Medicine, Japan

Multiple myeloma (MM) is an incurable hematological malignancy, despite recent development of novel moleculartargeted drugs. Elevated expression of PDZ binding kinase (PBK) has been reported to link to a poor prognosis in solidcancers, including gastric cancer and hepatocellular carcinoma. Here, we investigated the role of PBK in tumorigenesisof MM cells. Comprehensive cDNA microarray analysis showed that PBK expression readily increased after treatment
with intereukin-6, which is known as a key survival factor for MM cells. Importantly, the public data showed that theMM patients with higher expression of PBK have a significant shorter survival time compared with those with moderate/
lower expression of PBK. In addition, knockout of PBK gene dramatically suppressed tumor growth in KMS-11 cells
both in vitro and in vivo. We furtherer investigated the effect of PBK/rs3779620 genotype on tumorigenicity of MM
cells and found that PBK expression but not the genotype is related to tumor cell growth. Mechanistically, loss of PBK
increased the number of apoptotic cells and caspase-3 activity with concomitant decrease in the phosphorylation level of
Stat3. Interestingly, xenograft experiment showed that a novel PBK inhibitor OTS514 treatment significantly decreases
the KMS-11-derived tumor growth, compared to vehicle treatment. Taken together, these results indicate the possibility
that PBK expression is closely associated with myeloma tumorigenesis; PBK may be a novel therapeutic target for thetreatment of MM.

98

ポスター発表（Poster Presentation）
ポスター４

P4-3

温熱療法による骨髄腫細胞の TRAIL 感受性の亢進
Sensitization of myeloma cells to a TRAIL-mediated immunotherapy with hyperthermia

三木 浩和 1、中村 信元 2、Bat-Erdene Ariunzaya2、天真 寛文 3、小田 明日香 2、寺町 順平 4、岡本 恵暢 2、大浦 雅博 2、曽我部 公子 2、髙橋 真美子 2、岩佐 昌美 2、宇髙 憲吾 2、原田 武志 2、藤井 志朗 2、賀川 久美子 2、
安倍 正博 2
Hirokazu Miki1, Shingen Nakamura2, Bat-Erdene Ariunzaya2, Hirofumi Tenshin3, Asuka Oda2, Jumpei Teramachi4,

Yasunobu Okamoto2, Masahiro Oura2, Kimiko Sogabe2, Mamiko Takahashi2, Masami Iwasa2, Kengo Udaka2, Takeshi Harada2,
Shiro Fujii2, Kumiko Kagawa2, Masahiro Abe2

1

徳島大学病院 輸血・細胞治療部、2徳島大学大学院医歯薬学研究部 血液・内分泌代謝内科学、
徳島大学大学院医歯薬学研究部 口腔顎顔面矯正学分野、4徳島大学大学院医歯薬学研究部 口腔組織学分野

3

Division of Transfusion Medicine and Cell Therapy, Tokushima University Hospital, Tokushima, Japan, 2Department of

1

Hematology, Endocrinology and Metabolism, Institute of Biomedical Sciences, Tokushima University Graduate School,

Tokushima, Japan, 3Department of Orthodontics and Dentofacial Orthopedics, Tokushima University Graduate School of Oral

Sciences, Tokushima, Japan, 4Department of Tissue Regeneration, Tokushima University Graduate School of Oral Sciences,

Tokushima, Japan

Extramedullary disease is a major issue to be solved in multiple myeloma (MM). We recently developed novel
superparamagnetic nanoparticles which accumulate in extramedullary tumors and extirpate them and their progenitors
by heat generated with magnetic resonance. TNF-related apoptosis-inducing ligand (TRAIL) is induced in immune
effector cells activated in various immunotherapies. In the present study, we aimed to clarify the effects of hyperthermia
on TRAIL receptor editing and its downstream signaling in MM cells. Hyperthermia up-regulated endoplasmic reticulum
stress mediators, ATF4 and CHOP, along with DR5, a CHOP-target gene, in MM cells. Besides TRAIL receptor
expression, c-FLIP, a caspase 8 inhibitor to block DISC formation, is another critical determinant of TRAIL-induced
apoptosis. Heat treatment reduced the c-FLIP levels in MM cells at mRNA and protein levels, and cooperatively induced
MM cell death in combination with TRAIL. Hyperthermia and TRAIL synergistically induced caspase-8 activationand Sp1 reduction, and thereby markedly suppressed Sp1 driven pro-survival factors, IRF4 and c-Myc, in MM cells
in combination with TRAIL. Interestingly, caspase-8 inhibition suppressed heat- and TRAIL-induced Sp1 protein
degradation; and Sp1 inhibition reduced c-FLIP expression in MM cells, indicating caspase 8-mediated enzymatic Sp1degradation and thereby suppression of c-FLIP expression. These results suggest that hyperthermia not only directly
impairs MM cells but also may potentiate the efficacy of immunotherapies through MM cell sensitization to TRAIL.

99

ポスター発表（Poster Presentation）㊝ P4-4

HDAC1-IRF4-PIM2 経路を標的とする新規抗骨髄腫療法の開発
The novel therapeutic strategy targeting the HDAC1-IRF4-PIM2 pathway in myeloma cells

原田 武志 1、小田 明日香 2、天眞 寛文 3、寺町 順平 4、大浦 雅博 1、曽我部 公子 1、岩佐
中村 信元 2、三木 浩和 5、賀川 久美子 1、秀島 輝 6、Kenneth Anderson6、安倍 正博 2

昌美 2、藤井志朗 2、Takeshi Harada1, Asuka Oda2, Hirofumi Tenshin3, Jumpei Teramachi4, Masahiro Oura1, Kimiko Sogabe1, Masami Iwasa2,

Shiro Fujii2, Shingen Nakamura2, Hirokazu Miki5, Kumiko Kagawa1, Teru Hideshima6, Kenneth Anderson6, Masahiro Abe2

1

徳島大学病院 血液内科、2徳島大学大学院 医歯薬学研究部 血液・内分泌代謝内科学、
徳島大学大学院 医歯薬学研究部 口腔顎顔面矯正学、4徳島大学大学院 医歯薬学研究部 組織再生制御学、
5
徳島大学病院 輸血・細胞治療部、6ハーバード大学医学部 ダナ・ファーバー癌研究所
3

Department of Hematology, Tokushima University Hospital, Japan, 2Department of Hematology, Endocrinology and1Metabolism, Institute of Biomedical Sciences, Tokushima University Graduate School, Japan, 3Department of Orthodontics and

Dentofacial Orthopedics, Institute of Biomedical Sciences, Tokushima University Graduate School, Japan, 4Department of Tissue

Regeneration, Tokushima University Graduate School, Japan, 5Division of Transfusion Medicine and Cell Therapy, Tokushima

University Hospital, Japan, 6Jerome Lipper Myeloma Center, Dana-Farber Cancer Institute, Harvard Medical School, USA

HDAC1 is significantly elevated along with multiple myeloma (MM) progression from MGUS (GSE5900 & 2113).
IRF4 is a master transcription factor in MM cells and PIM2 is a critical kinase for MM-growth and bone metabolism.
Importantly, we found that HDAC1 downregulation/inhibition by shRNA or the class-I HDAC inhibitor MS-275
downregulated IRF4 and PIM2 in MM cell lines. In the present study, we aimed to clarify an essential molecularmechanism of HDAC1 inhibition-mediated modulation of IRF4-PIM2 axis. HDAC1 knockdown suppressed the growthof RPMI 8226 cells; however, IRF4 overexpression overcame the growth inhibitory effect, suggesting that IRF4 is adominant downstream target of HDAC1 inhibition-mediated MM cell growth inhibition. To delineate the machineryof HDAC1 inhibition-induced IRF4 downregulation, we focused on histone-acetylation balance in MM cells. IRF4
expression was reduced not only by MS-275, but also a histone acetyltransferase p300 inhibitor C646. These datasuggest that histone deacetylation, which generally upregulates silenced-gene expression, leads to downregulationof transcriptionally active genes. We then confirmed that PIM2 was transcriptionally regulated by IRF4 using ChIPSeq (GSE22901), ChIP-Q-PCR, and IRF4 knockdown. Based on these findings, we developed the synergistic growth
inhibitory effect by MS-275 in combination with the PIM inhibitor SMI-16a on MM cell lines and primary MM cells.
Taken together, targeting the HDAC1-IRF4-PIM2 axis by class-I HDAC inhibition in combination with PIM inhibition
may represent a novel treatment strategy in MM.

100

ポスター発表（Poster Presentation）

河野

和 1、稲田

ポスター４

P4-5

形質細胞特異的な代謝関連分子を標的とした多発性骨髄腫の治療開発研究
Targeting AMPD1, a plasma cell specific metabolic molecule, for multiple myeloma
treatment
優紀 2、笹野孝行 2、西村

直 1、松下豊 2、畑裕之 2、松岡雅雄 1

Yawara Kawano1, Yuki Inada2, Takayuki Sasano2, Nao Nishimura1, Yutaka Matsushita2, Hiroyuki Hata2, Masao Matsuoka1
1

熊本大学医学部附属病院 血液・膠原病・感染症内科、2熊本大学生命科学研究部生体情報解析学分野

Departments of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Hospital, Japan, 2Division of1

Informative Clinical Sciences, Faculty of Medical Sciences, Kumamoto University, Japan

Introduction: In order to achieve a cure in multiple myeloma (MM), it is necessary to develop new therapeutic strategies
highly specific to MM cells and targets unique pathways distinct from the present anti-myeloma agents. In the present
study, we attempt to identify a molecule specifically expressed in MM cells, and to examine its possibility as a novel
target for MM therapy.
Methods: Publically available gene expression websites were utilized in order to identify genes specifically expressedin normal plasma cells and MM cells. Gene and protein expression were analyzed by RT-PCR, Western blot andimmunohistochemistry. Cell viability post drug treatment were examined by flow-cytometry.
Results: AMPD1, a purine metabolic enzyme that converts AMP to IMP, was identified as a gene specifically expressedin normal plasma cells and MM cells. We confirmed that AMPD1 gene and protein were actually expressed specificallyin MM cells. AMPD inhibitors induced cell death in MM cells, while the effect against PBMCs and bone marrow
lymphocytes were minimal. AMPD inhibitors were more effective against MM cell lines under hypoxic condition
compared to normoxic condition.
Conclusions: AMPD1 is specifically expressed in normal plasma cells and MM cells. AMPD inhibitors showed specificcytotoxicity on MM cells and those effects were enhanced under hypoxic condition, suggesting that AMPD1 inhibition
works more specifically in the bone marrow microenvironment. Our report raises the possibility that AMPD1 inhibition
can be a novel therapeutic strategy specifically targeting MM cells.

101ポスター発表（Poster Presentation）

P5-1
笹野

骨髄腫細胞に対する新規 PDK1 阻害剤 JX06 の有用性
JX06, a potent and selective PDK1 inhibitor, is highly promising in myeloma therapeuticstrategy

孝行 1、河野和 2、松下豊 1、松岡雅雄 2、畑裕之 1

Takayuki Sasano1, Yawara Kawano2, Yutaka Matsushita1, Masao Matsuoka2, Hiroyuki Hata1

1

熊本大学 保健学教育部 生命科学研究部生体情報解析学分野、2熊本大学医学部附属病院 血液・膠原病・感染症内科

Department of Health Education, Kumamoto university, Japan, 2Departments of Hematology, Rheumatology, and Infectious

1

Disease, Kumamoto University Hospital, Japan

Background: PDK1 (Pyruvate dehydrogenase kinase 1) is a glucose metabolism-related protein mainly induced by
HIF-1. PDK1 inactivates PDH (pyruvate dehydrogenase), enhances glycolysis and suppresses the citric acid cycle. We
previously reported that PDK1 inhibition is a potent therapeutic strategy in multiple myeloma (MM). In the present study,
we examined the efficacy and mechanism of action of JX06, a novel PDK1 inhibitor effective at low concentrations insolid tumors, against MM cells.
Methods: MM cell lines and primary MM cells were treated with JX06 in vitro. Cell growth inhibition and cell death
were examined by WST-8 assay and flow cytometry. Caspase 3 activity and phosphorylation of PDH were determined byWestern blot.
Results: JX06 suppressed cell growth of various MM cell lines and primary MM cells at low concentrations. MM cell
death by JX06 accompanied caspase 3 activation and this cell death was suppressed under addition of caspase inhibitor,
which demonstrated that JX06 induced apoptosis in myeloma cells. Moreover, phosphorylation of PDH, known as atarget of PDK1, was significantly suppressed under JX06 treatment, indicating that JX06 exerts anti-myeloma effect byinhibiting PDK1-PDH pathway.
Conclusion: We demonstrated that JX06 could induce apoptosis of MM cell lines and primary MM cells by inhibiting
PDK1 at low concentrations. PDK1 inhibitors, such as JX06, may offer a new therapeutic option in MM therapy. We are
currently analyzing changes of metabolic status in MM cells post JX06 treatment.

102

ポスター発表（Poster Presentation）㊝ P5-2

多発性骨髄腫治療抵抗性のバイオマーカーの探索
Establishment of diagnostic biomarkers for the relapsed/refractory multiple myeloma inpatients treated with lenalidomide-based therapies
寛 2、佐藤 広太 3、石田 禎夫 3、田村和明 2、東條 有伸 1,2、今井 陽一 2

秀人 4、半田寛 5、佐々木純 6、川俣

豊隆 2、
ポスター５

小林 真之 1、安井
牧山 純也 2、横山

Masayuki Kobayashi1, Hiroshi Yasui2, Kota Sato3, Tadao Ishida3, Hideto Tamura4, Hiroshi Handa5, Makoto Sasaki6,
Toyotaka Kawamata2, Junya Makiyama2, Kazuaki Yokoyama2, Arinobu Tojo1,2, Yoichi Imai2

1

東京大学医科学研究所 分子療法分野、2東京大学医科学研究所附属病院 血液腫瘍内科、
3
日本赤十字社医療センター 血液内科、4日本医科大学 血液内科、5群馬大学 血液内科、6順天堂大学 血液内科

Division of Molecular Therapy, The Institute of Medical Science, The University of Tokyo, Japan, 2Department of Hematology,

1

The Institute of Medical Science, The University of Tokyo, Japan, 3Department of Hematology, Japanese Red Cross Medical

Center, Japan, 4Division of Hematology, Nippon Medical School, Japan, 5Department of Hematology, Gunma University, Japan,
Department of Hematology, Juntendo University School of Medicine, Japan

6

While the advent of novel agents has improved the outcome for patients with multiple myeloma (MM), patients withhigh-risk features still have poor outcomes and management of relapsed/refractory (RR) cases remains challenging.
RRMM cases require prompt diagnosis and suitable treatment. However, diagnosis is not easy and requires
multidisciplinary approach, which may result in delayed treatment. To address this issue, we carried out a multicenter
study to identify diagnostic biomarkers for RRMM in patients treated with lenalidomide-based regimens. To date, 16
patients (DRd (N=15), VRd (N=1)) are enrolled. Bone marrow and buccal mucosa was obtained from the patients, andperipheral blood plasma was also collected monthly. We designed a RRMM specific custom panel of 22 genes (ATM,BIRC2, BRAF, CARD11, CCND1, CRBN, CUL4B, CYLD, DIS3, EGFR, FAM46C, FGFR3, IL6ST, IRF4, KRAS, NFKB2,
NRAS, RASA2, SP140, STAT3, TP53, and TRAF3) and performed next-generation sequencing (NGS) analysis in 4
patients. MM cells were purified from the patient’s bone marrow cells by sorting CD138 positive fraction, and DNA wasextracted from the collected MM cells. Tumor DNA was subjected to NGS analysis with matched control. As a result, 4possible driver mutations including NRAS-Q61K, a known oncogenic mutation was found in 2 cases. We are planning toanalyze 20 cases in total, and determine whether the circulating cell-free DNA (cfDNA) in the patient’s plasma carries
the same mutations. Moreover, we will validate the potential of cfDNA as a diagnostic biomarker in RRMM using digital
droplet PCR.

103

ポスター発表（Poster Presentation）㊝ P5-3

骨髄腫治療における Akt 阻害と PRC2 阻害の相乗効果
Akt Inhibition Synergizes with PRC2 inhibition in the treatment of Multiple Myeloma

Mohamed Rizk1,2、Ola Rizq2、大島基彦 1,2、中島やえ子 1,2、一色佑介 2、岩間厚志 1,2、三村尚也 3Mohamed Rizk , Ola Rizq , Motohiko Oshima , Yaeko Nakajima-Takagi , Yusuke Isshiki , Atsushi Iwama , Naoya Mimura3
1,2

2

1,2

1,2

2

1,2

1

東京大学医科学研究所 幹細胞治療研究センター 幹細胞分子医学、2千葉大学大学院医学研究院 細胞分子医学、3
千葉大学医学部附属病院 輸血・細胞療法部

Division of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical

1

Science, University of Tokyo, Japan, 2Department of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba

University, Japan , 3Chiba University Hospital, Japan

Enhanced activation of PI3K/Akt pathway and epigenetic regulation mediated by Polycomb Repressive Complex 2(PRC2) play crucial roles in the pathogenesis of multiple myeloma (MM). However, the exact crosstalk between Aktpathway and PRC2 components EZH2 and its homolog EZH1 as therapeutic targets has not yet been fully illustrated.
We investigated the epigenetic impact of Akt inhibition on MM cells and the possible combination with PRC2 inhibition
using EZH2/1 inhibitors. We found that TAS-117, a potent and selective Akt inhibitor, induced cytotoxicity in MM cellswith activated phospho-Akt and low/deleted PTEN levels. Importantly, TAS-117 downregulated EZH2 expression at bothmRNA and protein levels via the interference with pRb-E2F pathway; while H3K27me3 was retained or upregulated,
due to the compensatory upregulation of EZH1. Moreover, EZH1 knockdown sensitized MM cells to TAS-117-induced
cytotoxicity. Based on these observations, we combined TAS-117 with either a dual EZH2/1 inhibitor, UNC1999, or aselective EZH2 inhibitor, GSK126. The dual EZH2/1 inhibition, but not the selective EZH2 inhibition, synergisticallyenhanced TAS-117-induced cytotoxicity and provoked apoptosis of MM cells. Of note, the combination inactivated
MAPK pathway, which was upregulated after TAS-117 treatment, suggesting an additional mechanism for the synergism
between Akt and EZH2/1 inhibitors. Collectively, our results underpin a link between Akt signaling and epigenetic
alterations, which emphasizes the benefits of targeting both Akt pathway and PRC2 activities as a therapeutic option in
MM.

104

ポスター発表（Poster Presentation）

P5-4
安井

寛 1、東條

多発性骨髄腫における新規多価ペプチドワクチン PVX-410, PVX-024 の開発
Development of novel, multi-peptide-based cancer vaccine PVX-410 and PVX-024 formultiple myeloma
有伸 1、Jooeun Bae2、Doris Peterkin3、Nikhil Munshi2、Kenneth Anderson2
ポスター５

Hiroshi Yasui1, Arinobu Tojo1, Jooeun Bae2, Doris Peterkin3, Nikhil Munshi2, Kenneth Anderson2
1

東京大学医科学研究所 附属病院血液腫瘍内科、2Dana-Farber Cancer Institute, Harvard Medical School, MA, USA、
3
OncoPep Inc., MA, USA
Department of Hematology/Oncology, The Institute of Medical Science, The University of Tokyo, Japan, 2Dana-Farber Cancer

1

Institute, Harvard Medical School, MA, USA, 3OncoPep Inc., MA, USA

Since multiple myeloma (MM) remains incurable, a therapeutic preemptive strategy for MM which would stop progression
at an early, asymptomatic stage of the disease is urgently needed. Since the immune system plays a significant role in
the progression of smoldering MM (SMM) to symptomatic MM, novel immunotherapeutic approaches designed to stop
progression to MM is very appealing. The use of peptide-based vaccines to trigger a memory anti-MM response presents
multiple advantages over other treatment options, including low toxicity, ability to target multiple tumor antigens, use incombination treatment regimens, as well as ease and cost of manufacturing. Four HLA-A2 peptides derived from X-box
binding protein 2 (XBP1 spliced/unspliced), CD138 (Syndecan-1) and CS1 (SLAMF7), highly expressed antigens in
MM, have been identified and formulated in an investigational vaccine (PVX-410, OncoPep,Inc.). Importantly, a phase
1/2A study of PVX-410, both as a monotherapy and in combination with lenalidomide (Celgene,Inc.), in patients with
SMM at moderate and high risk for progression to active MM demonstrated a safe profile; moreover, peptide-specificmemory anti-MM responses were induced in all patients and enhanced by lenalidomide (ASH,2017). Importantly,
to expand the eligible patient population for vaccine treatment to Asian populations including Japanese patients, four
HLA-A24 restricted peptides against these same antigens have been identified and characterized in preclinical studies(DFCI). Future phase 1/2 studies are planned in MM for HLA A2 and A24 positive patients in Asia.

105

ポスター発表（Poster Presentation）

P5-5

新規フタルイミド体 TC11 はチューブリン重合阻害および MCL1 分解を介してセレブロン非依存的に骨髄腫細胞のアポトーシスを導く
A novel phenylphthalimide, TC11, inhibits tubulin polymerization and degrades MCL1
followed by apoptosis of myeloma cells without modulating cereblon

大澤 翔 1、市川 大樹 1、中村 美沙 1、室田
松下 麻衣子 1、柳川 弘志 2、服部 豊 1

若菜 1、不藤

拓海 1、辻宏樹 1、佐俣光一 1、藤橋

和也 1、

Sho Osawa1, Daiju Ichikawa1, Misa Nakamura1, Wakana Murota1, Takumi Futo1, Hiroki Tsuji1, Koichi Samata1,
Kazuya Fujihashi1, Maiko Matsushita1, Hiroshi Yanagawa2, Yutaka Hattori1

1

慶應義塾大学薬学部、2IDACセラノスティクス株式会社

Faculty of pharmacy, University of Keio, Japan, 2IDAC Theranostics Inc., Tokyo, Japan

1

Today, the immunomodulatory drugs (IMiDs) represented by Lenalidomide play an important role in multiple myeloma(MM) treatment. However, the prognosis of MM in patients harboring cytogenetic abnormalities (CA) remains poor
despite recent advances in drug development that include the use of IMiDs. To overcome this issue, we have developed anovel phenylphthalimide, TC11, which is structurally related to IMiDs. Unlike existing IMiDs, TC11 induces apoptosis
in MM cells with high-risk CA. We found that TC11 directly bound to α-tubulin and nucleophosmin-1, but the molecularmechanisms of apoptosis induction remain unclear. Here, we show that TC11 inhibits tubulin polymerization and aberrant
mitotic asters, leading to mitotic arrest, independent of cereblon (CRBN) pathway. In fact, while IMiDs mainly degrade
IKZF1/3 and CK1α in the MM cells when IMiDs induce apoptosis, TC11 didn’t show their degradation. Moreover,TC11 can induce apoptosis in the CRBN knockdown MM cells. Since TC11 doesn’t bind to CRBN, it is presumed that
TC11 doesn’t induce teratogenicity. We also revealed that TC11 induced activation of casepase-9 and degradation of
MCL1. Furthermore, we found that inhibition of CDK1 by CGP74514A prevented TC11-induced MCL1 degradation andcasepase-9 activation and suppressed apoptotic cell death. These results suggest that TC11 induces apoptotic cell death
via mitotic arrest. Since the mitotic check-point is considered p53-independent, our findings may hold promise for theuse of TC11 as a potential drug candidate for the treatment of p53-deleted high-risk MM.

106

ポスター発表（Poster Presentation）

P6-1
飯塚

多発性骨髄腫の経過中に発症し形質細胞腫との鑑別に苦慮した形質細胞様型浸潤性尿路上皮癌
Metastatic plasmacytoid urothelial carcinoma mimicking plasmacytoma in a patient withmultiple myeloma

弘子 1,2、岩尾憲明 2、小池

道明 2、野口雅章 1、小松

則夫 3

ポスター５

Hiroko Iiduka1,2, Noriaki Iwao2, Michiaki Koike2, Masaaki Noguchi1, Norio Komatsu31

順天堂大学医学部附属浦安病院 血液内科、2順天堂大学医学部附属静岡病院 血液内科、
3
順天堂大学医学部内科学血液学講座

Department of Hematology, Juntendo University Urayasu Hospital, Japan, 2Department of Hematology, Juntendo University

1

Plasmacytoid urothelial carcinoma (PUC), is a rare histological type of urothelial carcinoma express CD138 similar
to plasma cells and is an aggressive variant associated with a poor prognosis. We present a case of PUC developed
during treatment of multiple myeloma (MM) and difficult differentiation from plasmacytoma. A 85-year-old woman
was referred to our hospital due to anemia in 20XX. Detailed examination led to a diagnosis of ISS III MM (IgA-λ),and she received VMP (bortezomib + melphalan + prednisolone) and Rd (lenalidomide + dexamethasone). Intermittent
hematuria was observed in April 20XX +2, and she was immediately hospitalized in May. Computed tomography
revealed a left kidney tumor and hematoma. We performed transcatheter arterial embolization for bleeding control. The
same time, she presented multiple cutaneous tumors and histopathological findings showed plasmacytoid cells, whichwere immunohistochemically positive to CD138. We diagnosed plasmacytoma, then radiotherapy was performed, which
resulted in a disappearance of the hematuria in June. However, she died due to severe acute cerebral infarction after 37
days of hospitalization. An autopsy examination showed multiple tumors of the kidney, liver, heart, lung, retroperitoneal
and mesentery. Immunohistochemical profiles were positive for AE1/3, CK7 and p40 compatible with PUC. This is apotential pitfall when dealing with cytologically obtained plasmacytoid malignancies. Immunohistochemical stains canbe helpful in sorting through the differential diagnosis, as PUCs are positive for epithelial markers.

107

ポスター６

Shizuoka Hospital, Japan, 3Department of Hematology, Juntendo University, Japan

ポスター発表（Poster Presentation）

P6-2
鈴木

IgA 血管炎の経過中に発症した Plasmablastic plasma cell myeloma の一例
A case of plasmablastic plasma cell myeloma developed during IgA vasculitis treatment

利貴央、川井

英嗣、古谷

大輔、小川

吉明、川田

浩志、安藤

潔

Rikio Suzuki, Hidetsugu Kawai, Daisuke Furuya, Yoshiaki Ogawa, Hiroshi Kawada, Kiyoshi Ando

東海大学医学部 血液・腫瘍内科

Department of Hematology/Oncology, Tokai University School of Medicine, Japan

A 74-year-old woman was referred to hospital because she developed a recurrent purpura on her whole body in
20XX. A skin biopsy demonstrated IgA-associated leukocytoclastic vasculitis (IgA LCV). After treatment with oral
prednisolone (PSL) therapy with some response, she developed renal dysfunction in November 20XX+1. The kidney
biopsy demonstrated crescent-forming glomerulonephritis as an IgA vasculitis lesion. After treatment with PSL,
tacrolimus, cyclophosphamide and azathioprine, she was referred to the Rheumatology Department of our hospital inJune 20XX+3 for the management of progressive renal dysfunction. Her renal function was stable after two cycles ofrituximab therapy and PSL oral administration. However, serum IgG was markedly elevated at 4487 mg/L with highserum LDH levels during the treatment. Therefore, she was referred to our department in November 20XX+3. She wasdiagnosed with plasmablastic plasma cell myeloma (PBPCM) IgG κ-type R-ISS stage III. Immunohistological study
revealed an increased number of plasmablasts expressing high levels of MYC in the bone marrow. FISH analysis ofbone marrow cells showed no high-risk factors. She started chemotherapy with Bd (bortezomib and dexamethasone) in
January 20XX+4. PBPCM shares many morphologic features with plasmablastic lymphoma (PBL), and generally shows
aggressive clinical course and poor prognosis. On the other hand, IgA LCV is known to be rarely complicated with IgA
multiple myeloma due to IgA deposition on the vascular walls. We will discuss the relationship between IgA LCV andIgG PBPCM.

108

ポスター発表（Poster Presentation）

P6-3
金杉

丈、加藤

閉塞性黄疸を合併し、胆管癌を疑われた形質細胞腫の 1 例
A case of plasmacytoma suspected of cholangiocarcinoma complicated by obstructive
jaundice
千絵、伊藤公人

Jo Kanasugi, Chie Kato, Masato Ito

大同病院 血液・化学療法内科

Division of Hematology/chemotherapy, Daido Hospital, Japan

109

ポスター６

CASE HISTORY: A 84 years old man presented with malaise and loss of appetite. He had polymyalgia rheumatica. He
had a high CRP value and got tired easily.PERTINENT FINDINGS: On physical examination, his body temperature
was 36.4 °C, blood pressure was 184/109 mmHg, heart rate was 104 beats/min, breathing frequency was 15 times /minute, and SpO2 was 97% (room air). Some laboratory data showed a very high value, such as calcium of 14.2mg/dL,
IgA of 2661 mg/dL. Hemoglobin level was 10.2 g/dl, and creatinine level was 1.24 mg/dL. Bone marrow examination
showed many plasma cell. Abdominal ultrasonography showed high luminance and nonuniform wall thickening in the
gallbladder neck. On abdominal computed tomography, low absorption masses were found in the neck of the gallbladder.
DIAGNOSIS and DISCUSSION: Based on these test results, it was diagnosed as multiple myeloma (ISS stage 3).
Treatment was initiated with lenalidomide and dexamethasone. Total protein and calcium decreased after treatment
started. More than 80% of plasmacytoma are distributed in the upper airway and upper gastrointestinal tract, and in theupper airway there are many paranasal sinuses. However, this case did not match. The tumor became smaller, so it turned
out to be a plasmacytoma but not a cholangiocarcinoma in this case. CONCLUSION: Extramedullary plasmacytoma
lacks characteristic findings in images and biochemical examinations, preoperative diagnosis is often not achieved. We
reported a case of plasmacytoma suspected of cholangiocarcinoma complicated by obstructive jaundice.

ポスター発表（Poster Presentation）

P6-4

NSD2/MMSET 発現は形質芽細胞腫瘍の鑑別に有用か？
Is NSD2/MMSET expression useful for the diagnosis of the plasmablastic neoplasms?

藤浪 春菜 1、木下
正木 彩子 2、伊藤史緒里 1、大島 佳子 1、菊池 隆希 1、鈴木 智貴 1、戸谷 治仁 1、浅尾旭 1、李 政樹 1、楠本 茂 1、小松 弘和 1、稲垣 宏 2、飯田 真介 1

優 1、成田朋子 1、Haruna Fujinami1, Shiori Kinoshita1, Yoshiko Oshima1, Takaki Kikuchi1, Tomotaka Suzuki1, Haruhito Totani1, Yu Asao1,
Tomoko Narita1, Ayako Masaki2, Asahi Ito1, Masaki Ri1, Shigeru Kusumoto1, Hirokazu Komatsu1, Hiroshi Inagaki2,
Shinsuke Iida1

1

名古屋市立大学 医学部 血液・腫瘍内科、2名古屋市立大学 医学部 臨床病理学

Hematology and Oncology, Nagoya City University, Nagoya, Japan, 2Pathology and Molecular Diagnostics, Nagoya City

1

University, Nagoya, Japan

A 69-year-old man presented with increase of subcutaneous masses and right lower leg neuropathy. FDG-PET showedabnormal uptake in multiple lymph nodes, subcutaneous masses, bone, lung and spleen. The patient was referred to ourdepartment because subcutaneous lesion biopsies showed suspicion of malignant lymphoma. The sacral lesion developed
into the spinal canal caused his right lower leg neuropathy. High-dose dexamethasone was given, whereas his leg
neuropathy progressed. Then, chemotherapeutic regimen with local irradiation for malignant lymphoma was given until
definitive pathological diagnosis. The histological diagnosis was difficult to distinguish between plasmablastic lymphoma(PBL) and multiple plasmacytoma (MP) with plasmablastic morphology. He had no immunodeficiency history andpresented high level of soluble IL-2 receptor and paraprotein in both serum and urine. There are no increase of atypicallymphocytes or plasma cells in bone marrow. One of subcutaneous biopsy showed proliferation of large atypical cells
which had plasmablast-like appearance with eccentrically placed nuclei and the other showed proliferation of relatively
differentiated plasma cells. Tumor cells showed positivity for CD20, CD138 and NSD2/MMSET and negativity for CD3
and EBER. Finally, we planned bortezomib based induction treatment followed by autologous stem-cell transplantation
based on the diagnosis of MP. Difficulty in the differential diagnosis between PBL and multiple myeloma or MP has beenreported. In this case, MMSET immunostaining could help deciding his treatment strategy.

110ポスター発表（Poster Presentation）

P6-5

t(11;14) 陽性多発性骨髄腫患者の臨床的病理学的な特徴
Clinicopathological analysis of multiple myeloma carrying t(11;14)

安藤 知恵 1、小林 宏紀 2、名塚
竹内 正美 2、末永 孝生 2

隆 1、村田翼 1、安部

佳亮 2、三浦大典 2、成田健太郎 2、北舘

明宏 2、

Tomoe Ando1, Hiroki Kobayashi2, Takashi Natsuka1, Tsubasa Murata1, Yoshiaki Abe2, Daisuke Miura2, Kenataro Narita2,
Akihiro Kitadate2, Masami Takeuchi2, Kosei Matsue2

1

亀田総合病院 臨床検査部、2亀田総合病院 血液腫瘍内科

Department of clinical laboratory, Kameda Medical Center, Japan, 2Division of Hematology/Oncology, Department of medicine,

1

Purpose: t(11;14) is common chromosome translocation in MM, but its clinicopathologic features in Japanese patientsremained unknown. This study aimed to clarify the clinicopathologic features of Japanese patients with t(11;14) MM.
Patients and Methods: We identified 221 patients with MM whose FISH studies were available. FISH was performedon the marrow aspirate samples until 2015 but on the purified CD138-positive cells thereafter. Surface marker analysis
was performed by 8-color FCM at diagnosis on all of the patients. Other laboratory data were extracted from the medical
records of our hospital.
Results: t(11;14) was detected in 53 (24%) patients. t(11;14) MM had more BJ type (P=0.016) and less IgG type (P=0.027)
compared to non-t(11;14) MM. FCM analysis revealed that t(11;14) MM was more likely to express the CD20 (16% vs
6%, P=0.043) and less likely to express CD56 (54% vs 22%, P<0.001) compare to non-t(11;14) MM. Of note, among the
8 patients with CD20-positive and t(11;14)-positive MM, 4 patient had small mature lymphocyte-like and 2 patients had
small basophilic erythroblast-like morphology. In contrast, all of the patients with CD20-positive non-t(11;14) MM had
typical plasma cell morphology. Although not statistically significant, patients with t(11;14) MM tended to have better
OS and PFS compared to those without t(11;14) and high-risk cytogenetics.
Conclusions: These observations indicate that, despite the heterogeneity, t(11;14)-positive MM may be a unique subsetof MM regarding surface markers and morphology.

111

ポスター６

Kameda Medical Center, Japan

ポスター発表（Poster Presentation）

P7-1
吉田

嵩 1、古田多発性骨髄腫に対する Daratumumab 療法と大腸癌に対する FOLFOX/FOLFIRI 療法を安全に併行しえた一例
A case successfully treated with concurrent chemotherapy of daratumumab for multiple
myeloma and bevacizumab-FOLFOX/FOLFIRI therapy for colon cancer
竜一 1、鈴木奈々 1,2、平出賢太郎 1、片岡孝江 1、伊奈

研次 1、粥川哲1

Takashi Yoshida1, Ryuichi Furuta1, Nana Suzuki1,2, Kentaro Hirade1, Takae Kataoka1, Kenji Ina1, Satoshi Kayukawa1
1

名古屋記念病院 血液・化学療法内科、2名古屋市立大学大学院医学研究科 血液・腫瘍内科学分野

Department of Clinical Oncology, Nagoya Memorial Hospital, Japan, 2Department of Hematology & Oncology, Nagoya City

1

University Graduate School of Medical Sciences, Japan

Recent progress in chemotherapy for multiple myeloma (MM) brings favorable prognosis, but some patients suffer fromother malignancies. Managing such cases with multiple malignancy is difficult, but the optimal treatment should beselected considering the benefit of patients. We experienced a case with refractory MM complicated by colon cancer (CC),whose both malignancies were successfully treated.
A 74-year male was diagnosed with MM in X-5 years ago and received 9 cycles of melphalan, prednisolone, andbortezomib therapy. After relapse he was treated with lenalidomide and dexamethasone (Ld) for 4 cycles. A year later,
his MM recurred and imaging studies showed complication of CC. He underwent curative resection, but metastatic
liver tumor was identified, which were curatively resected. He was treated with elotuzumab in combination with Ld
during the procedures. Unfortunately his CC re-relapsed and MM showed partial response in X year. BevacizumabFOLFOX (5-FU, folinate, and oxaliplatin) therapy was initiated for the treatment of metastatic CC and elotuzumab waschanged to daratumumab in combination with Ld. While lenalidomide was ceased because of neutropenia, FOLFOX
was consequently switched to FOLFIRI (5-FU, folinate, and irinotecan) which yielded to partial response. MM reachedcomplete response in X+1 year.
Our case showed efficacy and safety of concurrent chemotherapy of daratumumab and bevacizumab-FOLFOX/FOLFIRI
therapy. It is implicated our experience provide useful information to determine the line of treatment for MM associatedwith other malignancies.

112ポスター発表（Poster Presentation）

P7-2
山田
浅野

自家移植が困難である再発難治性 MM に対する Tandem での血縁者 HLA 一致同種移植実施の効果と安全性に対する考察
Tandem allogeneic stem cell transplantation from an HLA matched sibling donor for
relapsed/refractory multiple myeloma

晃子、赤羽 大悟、藤本 博昭、伊藤 良和、後藤 守孝、大月 俊輔、森山 充、齊藤倫代、勝呂 多光子、吉澤 成一郎、田中 裕子、古屋 奈穂子、大屋敷 一馬

優、片桐

誠一朗、

Akiko Yamada, Daigo Akahane, Hiroaki Fujimoto, yoshikazu Itoh, Moritaka Gotoh, Shunsuke Otsuki, Mitsuru Moriyama,
Yuu Saitoh, Seiichiro Katagiri, Michiyo Asano, Tamiko Suguro, Seiichiro Yoshizawa, Yuko Tanaka, Nahoko Furuya,
Kazuma Ohyashiki

東京医科大学病院 血液内科

Department of hematology, Tokyo Medical University, Japan«Case report» A 44-year-old man diagnosed as MM (BJP-k, ISS1, del(17p)) received treatments of Bd, VRd, Kd, KRd,
Pd, KPd, ERd, D-CEP, DRd and IRd with focal irradiation. However, he failed to achieve remission by any of them.
He underwent allo-SCT at the age of 45 from an HLA-identical sister (employing Flu 125 mg/m2, Mel 140 mg/m2and
TBI 4Gy for preconditioning, and CsA and short term MTX for GVHD prophylaxis). Although normalization of freelight chain accompanied by grade II aGVHD were observed, newly plasmacytomas appeared on his forehead 4 months
after the transplant. Then, focal irradiation (30Gy) and IRd therapy brought him PR. Fortunately there were stem cells
remaining, so we performed 2nd allo-SCT from the same donor (employing MEAM regimen and CsA for GVHD
prophylaxis) 230 days after 1st allo-SCT. He achieved the first CR after 2nd allo-SCT.
«Conclusion» Allo-SCT from a sibling donor should be considered for young patients with highly refractory MM. Recent
technical progress might increase its feasibility. More discussion about allo-SCT for RRMM will be expected.

113

ポスター７

«Introduction» Indication of allogeneic (allo) hematopoietic stem cell transplantation (SCT) for multiple myeloma (MM)is still controversial because of high transplant-related mortality (TRM). But it remains as a potentially curative treatment
for some cases. Here we report a case with relapsed/refractory MM (RRMM) obtaining some benefit after tandem alloSCTs.

ポスター発表（Poster Presentation）

P7-3
伊藤
高橋

IRd（ixazomib, lenalidomide and dexamethasone）療法開始後早期に腫瘍崩壊症候群を起こした再発難治性骨髄腫
Tumor lysis syndrome (TLS) caused by IRd regimen in a patient with relapsed/refractory
multiple myeloma

俊輔、宇賀田 典美、島崎 裕正、岡田 祐介、高橋
勉、三宅 隆明、鈴木 律朗、鈴宮 淳司

史匡、藤本

亜弓、松田

真一朗、岡田隆宏、池尻文良、Shunsuke Ito, Norimi Ugata, Yasumasa Shimasaki, Yusuke Okada, Fumimasa Takahashi, Ayumi Fujimoto,Shinichiro Matsuda, Takahiro Okada, Fumiyoshi Ikejiri, Tsutomu Takahashi, Takaaki Miyake, Ritsuro Suzuki, Junji Suzumiya

島根大学医学部附属病院 腫瘍・血液内科

Department of Oncology/Hematology, Innovative cancer center, Shimane University Hospital, Japan【Introduction】Multiple myeloma is considered as a low-risk disease of TLS. However, in recent era, there are several
reports of TLS associated with novel agents such as bortezomib. We experienced a case of TLS with IRd therapy.
【Case】A 70-year-old woman was diagnosed with multiple myeloma 9 years ago. She was initially treated with Bd,
followed by thalidomide and Rd regimen and achieved sCR. She experienced relapse of myeloma 3 years after initial
treatment, and then received thalidomide and lenalidomide. However, her myeloma was assessed as refractory after
6-year use of lenalidomide therapy. At the time of current presentation, her laboratory data were as follows: Ca 10.2 mg/
dl, P 3.5 mg/dl, BUN 25.6 mg/dl, Crea 1.07 mg/dl, uric acid 5.0 mg/dl, IgG 2514 mg/dl, and serum FLC ratio 736.5. The
bone marrow examination showed 66.2% plasma cells, and del(17p) karyotype by FISH. A salvage treatment with IRd
regimen was initiated. On the following day of treatment initiation, she developed hyperphosphatemia, hypocalcemia,
hyperuricemia, acute kidney injury and anuria. A diagnosis of TLS was made. IRd treatment was stopped, and continuous
hemodiafiltration was started. The TLS was successfully relieved. IRd regimen was administered only for 1 day, it was
highly effective with lowering IgG and improving FLC ratio.
【Discussion】In this case, massive TLS occurred in a short time. TLS in IRd regimen has not been reported, andtherefore is considered as a rare adverse event. Predictive markers of TLS should be investigated in the era of effective
molecular targeted agents.

114

ポスター発表（Poster Presentation）㊝ P7-4
工藤

Carfilzomib で溶血 /TMA に至った多発性骨髄腫の 3 例
Three myeloma patients complicated by calfilzomib-related hemolysis or TMA

大輔 1、岡崎幸治 1、奥田優子 1、平井理泉 1、谷村

聡 1、竹下昌孝 1,2、三輪

哲義 1,2

Daisuke Kudo , Koji Okazaki , Yuko Okuda , Risen Hirai , Akira Tanimura , Masataka Takeshita , Akiyoshi Miwa1,2
1

1

1

1

1

1,2

1

東京北医療センター 血液内科、2国際骨髄腫先端治療研究センター

Department of hematology, Tokyo-kita Medical Center, Japan, 2International Myeloma Center for Advanced Reseach and

1Treatment, Japan

115

ポスター７

Introduction: Carfilzomib(CFZ)-related hemolysis including TMA was reported at times. We explained three myeloma
patients complicated by CFZ-related hemolysis among 29 patients receiving CFZ from Apr 2017 to Dec 2018.
Case 1: A 68-year-old man was treated with Kd. At cycle 2 day 15, hemolysis was detected ( Hb 9.3 g/dl, LDH 319 U/l,ID-bil 1.7mg/dl, haptoglobin (HPT) < 10 mg/dl ) with blood schistocytes and negative Coomb`s test. Thrombocytopenia
and serum creatinine elevation were not detected. The diagnosis of TMA was made, which resulted in cessation of Kd.
Although his anemia was progressed, RBC transfusion was not required. His blood counts recovered after 15 days.
Case 2: A 57-year-old man was treated with Kd. At cycle 3 day 9, hemolysis was detected ( Hb 9.5 g/dl, LDH 344 U/l, ID-bil 2.2 mg/dl, HPT < 10 mg/dl ) with negative Coomb`s test. Schistocytes, thrombocytopenia or serum creatinine
elevation was not detected. Kd was skipped on day9, reduced on day15/16. His blood counts recovered after 14 days.
Case 3: A 63-year-old female was treated with KRd. At cycle 3 day 15, hemolysis was detected ( Hb 10.2 g/dl, LDH 246
U/l, ID-bil 1.3mg/dl, HPT < 10 mg/dl ). Schistocytes, thrombocytopenia or serum creatinine elevation was not detected.
She completed treatment until cycle 4 due to no worsening. Her blood counts recovered to baseline after 15 days.
Conclusion: Through clinical course, dose-dependent fashion, or immune-mediated mechanism could be suggested.
However, further analysis is needed to investigate the precise mechanism.

ポスター発表（Poster Presentation）

P7-5
入田
名取

博史、藤野
一彦

IgD λ骨髄腫の治療経験
Experience of IgD λ myeloma treatment
春香、長瀬

大輔、三井

ゆりか、廣田

愛、恩田

直輝、倉石

安庸、加藤

元浩、

Hirofumi Irita, Haruka Fujino, Daisuke Nagase, Yurika Mitsui, Ai Hirota, Naoki Onda, Yasunobu Kuraishi, Motohiro Kato,
Kazuhiko Natori

東邦大学医療センター大森病院 血液・腫瘍科

Division of Hematology and Oncology, Toho University Medical Center Oomori Hospital, Japan[Introduction] IgD multiple myeloma (MM) is a rare type of disease that accounts for 1-2% of all MMs. We report acase of IgDλ MM that we experienced.
[Case presentation] A 59-year-old male presented with the chief complaint of back pain. In August 20XX, the patient
experienced sudden back pain and was examined at a nearby clinic where he was found to have a thoracic compression
fracture and severe anemia. The patient was therefore referred to our department. Since laboratory tests revealed IgDlevels of 12400 mg/dl, IgDλ MM was diagnosed. Treatment with BD therapy was initiated, yielding a decrease in IgD.
However, after the 4th course was completed, IgD increased again, and treatment was therefore switched to CyBorD
therapy. Following the 6th course of CyBorD therapy, and from December 20XX+1, Rd therapy was introduced. After theend of the 8th course, on July 20XX+2, autoPBSCT was performed, resulting in partial remission. After the autoPBSCT,IgD levels increased and atypical lymphocytes (plasmocyte-like) appeared. In November, VRD therapy was initiated.
During follow-up, infection complicated the condition of the patient and he passed away after 28 months.
[Discussion] Compared to other MMs, IgD MM tends to occur in young people and has a poor prognosis. Even if
complete response is achieved with conventional chemotherapy, additional treatment with autoPBSCT is necessary to
improve the prognosis. Since this case, it has become possible to use several types of new therapeutic drugs. As such, theprognosis of IgD MM will likely improve in the future.

116

ポスター発表（Poster Presentation）

P8-1
内原

ダラツムマブと少量のレナリドミドの併用療法が奏功した治療抵抗性 IgD- λ型多発性骨髄腫の一例
A case of IgD- λ relapse/refractory multiple myeloma in which combination therapy withdaratumumab and low-dose lenalidomide was effective

潤之介、新垣均

Jun-nosuke Uchihara, Hitoshi Arakaki

那覇市立病院 血液内科

Department of hematology, Naha city hospital, Japan

ポスター７

Although daratumumab, lenalidomide, dexamethasone (DRd) is effective for relapse/refractory multiple myeloma(RRMM) in POLLUX study, cases that are sensitive to lenalidomide are targeted in this study. We report a IgD-λRRMM
patient, who showed resistance to lenalidomide previous treatment and responded well to daratumumab and low-dose
lenalidomide. The patient was a 64-year-old man, who diagnosed multiple myeloma, IgD -λtype in June 2014. He wastreated with bortezomib and dexamethasone therapy from July, but IgD did not change. The regimen was changed tolenalidomide, dexamethasone, IgD decreased to below sensitivity. Although myeloma was stable by the continuationof this therapy, IgD increased again from February 2018. Because judgment of relapse and changed the regimen was areaction failure, we started DRd from September. Due to impaired renal function, lenalidomide was reduced to 5mg/day.
IgD decreased again after one course of DRd, and this therapy is still continuing.

ポスター８

117

ポスター発表（Poster Presentation）

P8-2
奥田

優子、谷村

多発性骨髄腫に対する自家末梢血幹細胞移植において TMA を発症した一例
One clinical case of thrombotic microangiopathy developing after engraftment of auto stem
cell transplantation in multiple myeloma
聡、岡崎

幸治、平井

理泉、工藤

大輔、竹下

昌孝、三輪

哲義

Yuko Okuda, Akira Tanimura, Koji Okazaki, Risen Hirai, Daisuke Kudo, Masataka Takeshita, Akiyoshi Miwa

東京北医療センター 血液内科

Department of hematology, Tokyo kita medical center, Japan

There are few cases complicated by thrombotic microangiopathy(TMA) during autologous stem celltransplantation(ASCT) for multiple myeloma(MM).We present a myeloma case complicated by TMA developing during
ASCT, who was successfully treated with repetitive plasma exchange(PE)s. A 69 years old female, who was diagnosed
MM(IgAλ) followed by the first ASCT in 20XX-10. She was transferred due to myeloma relapse. Bortezomib containing
re-induction regimen was instituted. Following melphalan 140mg/m2 conditioning, sufficient number of stem cells wasinfused. We confirmed the engraftment on day 11.On day21 visual field defect and peliosis appeared. Thrombocytopenia
with refractoriness to platelet transfusion, hemolytic anemia, severe liver damageand schistocyte were observed and TMA
was diagnosed. Increased level of CRP and hyper polyclonal gamma-globulinemia suggested alternation of immune
system. Steroid pulse therapy, PE and rcombinant thombomodulin was administered. Although the ADMATS13 activity
was decreased under10%, inhibitor of ADAMTS13 was not detected and Von Wille brand factor multimer analysis werenormal, which might not be suggesting of immune-related thrombotic thrombocytopenic purpura. Full inspection forseveral microorganisms and auto-antibody analyses performed, which revealed no abnormality. The diagnosis of ASCTassociated TMA was established. Her symptoms showed gradual improvement during repetitive PEs. Three month later,
clnical finding compatible with TMA have disappeared completely, and besides, the MM attained stringent complete
response.

118

ポスター発表（Poster Presentation）

P8-3
池田

新規プロテアソーム阻害剤（Carfilzomib, Ixazomib) を投与した後再発した難治性骨髄腫に対して Daratumumab を使用した 4 症例
Efficacies of daratumumab in four patients with relapsed and refractory multiple myeloma
against new proteasome inhibitors (Carfilzomib, Ixazomib)

博 1、高田弘一 1,2、村瀬和幸 2、後藤亜香利 1、菊池尚平 1,2、井山

諭 1、加藤淳二 2、小船

Hiroshi Ikeda1, Kouichi Takada1,2, Kazuyuki Murase2, Akari Gotou1, Shouhei Kikuchi1,2, Satoshi Iyama1, Junji Katou2,

雅義 1

Masayoshi Kobune1

1
1

札幌医科大学医学部 血液内科、2札幌医科大学医学部 腫瘍内科

Department of hematology, Sapporo Medical University, Japan, 2 Department of oncology, Sapporo Medical University, Japan

119

ポスター８

(Introduction) Recently, novel antibodies are effective therapies for multiple myeloma (MM) and contributed tosignificant improvements in disease outcomes.Here, we show efficacies of treatment with daratumumab following
new proteasome inhibitors (Carfilzomib and Ixazomib ) in combined with immunomodulatory drugs in four patientswith relapsed/refractory MM (RRMM).(Case reports) Case1. 66-year-old female was diagnosed with smoldering MM
in 200X. She was treated with four cycles of Bortezomib+cyclophosphamide+DEX (VCD) and subsequently autoperipheral blood stem cell transplantation. She achieved complete response (CR). She relapsed in 200X+7 and treated
10 cycles of Ixazomib+Lenaridomide (R)+DEX (IRD). She administrated with 4 cycles of Daratumumab, R and DEX
therapy and achieved stringent CR (sCR). Case2. 73-years-old male was diagnosed Multiple myeloma IgA-k type(RISS stage Ⅲ del17p+)in 20Y. He was treated with three cycles of VCD and VRD and achieved sCR. He relapsed andtreated with 10 cycles of Pomalidomide+DEX(PD)in 20Y+4. However, IgA level was elevated during PD treatment andtreatment was changed to Carfilzomib+ R+DEX (KRD). RRMM was not responded to 15 cycles of KRD in 20Y+5.
Hence, he was administrated with Daratumumab,bortezomib and DEX therapy and achieved stringent CR after 4 cycleof treatment. (Results and Discussion) Daratuzumab showed a strong effect for patient with RRMM, even if patientswere refractory against new proteasome inhibitors in our experience. Importantly, there is no efficacy for patients over 5
regimens and extra-medurary plasmacytoma.

ポスター発表（Poster Presentation）

P8-4
王梓任 1、丸茂

再発難治性多発性骨髄腫に対してダラツムマブ併用 Ld 療法（DaraLd）で VGPR を達成し自家末梢幹細胞移植（ASCT）を施行できた一例
Successful salvage treatment using daratumumab combined with lenalidomide anddexamethasone in a patient with refractory multiple myeloma
義晃 1、森芙美子 1、楠本

茂 2、飯田真介 2、稲垣淳1

Ziren Wang1, Yoshiaki Marumo1, Fumiko Mori1, Shigeru Kusumoto2, Shinsuke Iida2, Atsushi Inagaki1
1

名古屋市立西部医療センター 血液腫瘍内科、2名古屋市立大学大学院医学研究科 血液・腫瘍内科学

Nagoya City West Medical Center, Department of Hematology and Oncology,Japan, 2Department of Hematology and1

Oncology, Nagoya City University Graduate School of Medical Sciences, Japan[Introduction] Anti-CD38 antibody, daratumumab (DARA) has been shown to be effective for relapsed/refractory
multiple myeloma (MM), however, there is limited evidence regarding the effectiveness of DARA for MM refractory tobortezomib and lenalidomide.
[Case] A 62-year-old woman presented with lower back pain, renal dysfunction, anemia and hypercalcemia. She wasdiagnosed as having BJP-λ-type symptomatic multiple myeloma, ISS stage Ⅲ . She immediately received weekly
bortezomib and low-dose dexamethasone (Bd), and achieved a complete response after 3 cycles of this therapy. Althoughautologous stem cell transplantation (ASCT) was recommended as a consolidation therapy, she desired to continue Bd
therapy. However, myeloma relapsed after 10 cycles of Bd, then 7 cycles of lenalidomide with low-dose dexamethasone(Ld) was given until progression. Despite giving 4 cycles of carfilzomib with dexamethasone (Kd) and 2 cycles ofdoxorubicin, bortezomib, dexamethasone (PAD) therapy for her relapsed/refractory myeloma, she failed to respond andthe myeloma rapidly progressed. Therefore, daratumumab in combination with Ld (DLd) therapy was selected as a 4thline salvage regimen for her refractory myeloma. She achieved a very good partial response after just one cycle of DLd
without any serious adverse events. Finally, she received high-dose melphalan followed by ASCT.
[Conclusion] DLd was an effective combination regimen for bridging to ASCT for multiple myeloma refractory to Bd,
Ld, Kd and PAD.

120

ポスター発表（Poster Presentation）

P8-5

Daratumumab 併用化学療法後に B 型肝炎ウイルス再活性化を認めた多発性骨髄腫の 1 例
Hepatitis B virus (HBV) reactivation in a myeloma patient with resolved HBV infection who
received daratumumab containing chemotherapy

菊池 隆希 1、楠本 茂 1、田中
浅尾 優 1、成田 朋子 1、伊藤

靖人 2、大島 佳子 1、藤浪 春菜 1、鈴木 智貴 1、戸谷旭 1、李 政樹 1、小松 弘和 1、飯田 真介 1

治仁 1、木下史緒理 1、

Takaki Kikuchi1, Shigeru Kusumoto1, Yasuhito Tanaka2, Yoshiko Oshima1, Haruna Fujinami1, Tomotaka Suzuki1,

Haruhito Totani1, Shiori Kinoshita1, Yu Asao1, Tomoko Narita1, Asahi Ito1, Masaki Ri1, Hirokazu Komatsu1, Shinsuke Iida1
1

名古屋市立大学大学院医学研究科 血液・腫瘍内科学、2名古屋市立大学大学院医学研究科 病態医科学

Department of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Japan, 2Department

1of Virology and Liver unit, Nagoya City University Graduate School of Medical Sciences, Japan

121

ポスター８

Introduction: There is extremely limited evidence regarding HBV reactivation in patients with multiple myeloma (MM)
who received anti-CD38 antibody, daratumumab (DARA).
Case: A 72-year-old woman was diagnosed with symptomatic MM in September 20XX. She was considered to haveresolved HBV infection because of the following HBV-related markers: HBsAg-negative, anti-HBc-positive, anti-HBsnegative and undetectable HBV DNA. She underwent regular HBV DNA monitoring during and after chemotherapy
for MM. She received bortezomib combined with melphalan and prednisone (MPB) as the initial chemotherapy
regimen from October 20XX but she had progressive disease (PD) after 3 cycles of MPB. Subsequently, she received
lenalidomide and dexamethasone (Ld) from January 20XX+1 but PD recurred in June 20XX+3. Because she desired tocontinue oral anti-MM treatment, pomalidomide and dexamethasone (Pd) treatment was selected, but PD recurred after
2 cycles of Pd. DARA combined with bortezomib and dexamethazone (DBd), as fourth line regimen, was started from
September 20XX+3. Unexpectedly, HBV reactivation was diagnosed when her HBV DNA levels suddenly increased to 2.2
Log IU/mL, after 3 cycles of DBd. At one week after HBV reactivation, she received preemptive anti-HBV therapy using
entecavir, at the peak HBV-DNA level of 2.6 Log IU/mL, without any HBV-related hepatitis.
Conclusion: DARA may be associated with an increased risk of HBV reactivation. Well-designed basic and clinicalresearch are warranted to clarify the mechanism and risk factors of HBV reactivation after DARA.

ポスター発表（Poster Presentation）

P9-1
丸茂

義晃 1、森骨生検と MYD88 変異解析で多発性骨髄腫と鑑別し得たリンパ形質細胞性リンパ腫の一例
Bone biopsy and MYD88 mutation analysis is useful for the diagnosis of lymphoplasmacytic
lymphoma with lytic bone lesions mimicking multiple myeloma
芙美子 1、楠本

茂 2、飯田真介 2、稲垣淳1

Yoshiaki Marumo1, Fumiko Mori1, Shigeru Kusumoto2, Shinsuke Iida2, Atsushi Inagaki1
1

名古屋市立西部医療センター 血液・腫瘍内科、2名古屋市立大学大学院医学研究科 血液・腫瘍内科学

Nagoya City West Medical Center, Hematology and Oncology, Japan, 2Department of Hematology and Oncology, Nagoya City

1

University Graduate School of Medical Sciences, Japan[Introduction] Lymphoplasmacytic lymphoma/Waldenstrom macroglobulinemia (LPL/WM) is a lymphoproliferative
neoplasm often presenting with anemia, renal insufficiency, or peripheral neuropathy. The incidence of lytic bone lesion
has been reported to be less than 5% in patients with LPL/WM and it is often difficult to distinguish such patients withosteolytic lesions from those with multiple myeloma.[Case] An 86-year-old man presented with worsening stinging
pain in both legs. He had been followed for chronic kidney disease (eGFR 45ml/min), and normocytic anemia for one
year. He had fallen from a chair because of numbness of his legs and had fractured his pubic bone, at which point he
was referred to our hospital. Magnetic resonance imaging of the pelvis and spine showed multiple lytic bone lesions iniliac bone and multiple vertebrae, which we suspected of multiple myeloma. Serum immunofixation revealed IgM-λtype monoclonal protein, but calcium concentration, serum free light chain ratio (κ/λ= 58.9/58.4) and urinary protein(0.03g/g creatinine) were in normal ranges. However, his serum sIL-2 receptor levels were markedly elevated at 4,391
U/mL. Then, he was diagnosed as having low-grade B cell lymphoma histologically by ileum biopsy showing CD10+,
CD19+, CD20+, CD23+, κ<<λ, CD38+, bcl-2+, CD138- cells consistent with LPL/WM. Finally, bone marrow aspiration
confirmed lymphoma involvement and MYD88 gene mutation was detected by PCR.[Conclusion] Bone biopsy and
MYD88 mutation analysis were useful to distinguish LPL/WM with lytic bone lesions from IgM-type multiple myeloma.

122ポスター発表（Poster Presentation）

P9-2
成田

IgG κ型リンパ形質細胞性リンパ腫に合併した軽鎖沈着症の一例
Light chain deposition disease associated with IgG- κ type lymphoplasmacytic lymphoma

健太郎、小林

宏紀、北舘

明宏、安部

佳亮、三浦

大輔、津島

隆史、竹内

正美、末永

孝生

Kentaro Narita, Hiroki Kobayashi, Akihiro Kitadate, Yoshiaki Abe, Daisuke Miura, Takafumi Tsushima, Masami Takeuchi,
Kosei Matsue

亀田総合病院 血液腫瘍内科

Division of Hematology/Oncology, Department of Medicine, Kameda Medical Center, Japan

Background: Light chain deposition disease (LCDD) is characterized by monotypic immunoglobulin (Ig) depositionin the kidney that will cause renal dysfunction. Although most of the patients with LCDD have underlying plasma cell
dyscrasia, patient with lymphoplasmacytic lymphoma (LPL) has rarely reported. Here we report the case of kidney
LCDD with IgG-κ type LPL.
Case presentation: A 62-year-old female was referred with nephrotic syndrome. Serum creatinine level was 1.95mg/
dL and eGFR was 21.12mL/min/1.73m2. Serum total protein and albumin level was decreased to 3.8g/dl and 2.1g/dl
respectively. Marked hypogammaglobulinemia with IgG 21mg/dL, IgA: 15.0mg/dL, IgM: 12.0mg/dL was observed.
Serum FLCκand FLCλwere 158mg/L and 5.9mg/L, respectively. Serum immunofixation (IFx) was negative atpresentation but it turned out positive for IgGκ later. Urine IFx was positive for Igκ light chain. Bone marrow biopsy
showed infiltration of monotonous small lymphocytes positive for CD20, but negative for CD5, CD10, BCL-6, andCD138. MYD88L265P mutation was positive on bone marrow sample. Kidney biopsy revealed the interstitial infiltrationof CD20-positive small lymphocytes and glomerular sclerosis consistent with membranoproliferative glomerulonephritis.
Immunofluorescence showed glomerular deposition of monoclonal Igκ chain. Electron microscopy showedsubendothelial ground-pepper-like electron dense deposits, which is compatible with light chain deposition disease. We
initiated the chemotherapy of R-CVP on the basis of the diagnosis of IgG-κ type lymphoplasmacytic lymphoma.
ポスター９

123

ポスター発表（Poster Presentation）

P9-3
入内島

アミオダロンと ICD により再発する pulseless VT 後も長期生存を得た全身性 AL アミロイドー
シスの 1 例
Long-term survival of an AL amyloidosis patient with recurrent pulseless VT treated with
amiodarone and implantable cardioverter defibrillator (ICD)

裕乃 1、石埼卓馬 1、吉田くに子 2、飯塚

貴士 2、田村峻太郎 2、村上博和 3、半田寛1

Hirono Iriuchishima1, Takuma Ishizaki1, Kuniko Yoshida2, Takashi Iizuka2, Shuntaro Tamura2, Hirokazu Murakami3,

Hiroshi Handa1
1

群馬大学医学部 血液内科、2群馬大学医学部 循環器内科、3群馬大学医学部保健学科 応用検査学

Department of Hematology, Gunma University Graduate School of Medicine, Gunma, Japan, 2Department of Cardiovascular1

Medicine, Gunma University Graduate School of Medicine, Gunma, Japan, 3Department of Laboratory Sciences, Gunma
University Graduate School of Health Sciences, Gunma, Japan【Introduction】Prognosis of symptomatic cardiac AL amyloidosis is poor due to a limited benefit of pharmacologic
treatment for heart failure and chemotherapy for amyloidosis. Here we report a case with systemic AL amyloidosis whodeveloped PEA and pulseless VT several times, but survive for relatively long term by ICD, amiodarone and melphalan+ dexamethasone (MD) therapy.【Case】A 60 year-old man with severe cardiac AL amyloidosis (NT-proBNP 2856 ng/
l, troponin T 0.0049μg/l) was treated with MD therapy from May 2017. Next month, he developed cessation of breathing
during sleep and PEA. Moreover, he experienced pulseless VT three times a couple of days in July 2017. He wastreated with amiodarone followed by ICD implantation. To support his cardiac function, he was prescribed mexiletine,
frosemide, and spironolactone. Then he received total 13 courses of MD therapy as outpatient without ICD operation. He
died of aggravation of both heart and renal failure in 18 months from diagnosis.【Discussion】Prognosis of systemic AL
amyloidosis with dominant cardiac involvement is generally very poor with median overall survival of 3.5 months (Mayostating system in 2004). The adaption of ICD for cardiac AL amyloidosis is unclear, and it did not operate in this case but
the effectiveness of ICD is shown by several studies that it is superior to amiodarone in preventing sudden death causedby lethal arrhythmia. We assume that the severe cardiac amyloidosis were successfully managed while maintaining goodquality of life by combination of amiodarone, ICD implantation and chemotherapy.

124

ポスター発表（Poster Presentation）

P9-4

心 AL アミロイドーシスに対するボルテゾミブ療法中に、洞停止や消化管出血などを発症した一例
Cardiac AL amyloidosis that developed sinus arrest and gastrointestinal bleeding during
Bortezomib +Dexamethasone (BD) therapy

寺川 拓弥 1、井上筒井 秀作 3

愛 1、高橋雅文 1、石田尚子 1、徳嶺進洋 1、嶋本

新作 2、下山寿 2、荻山秀治 3、Takuya Terakawa1, Megumu Inoue1, Masaaki Takahashi1, Naoko Ishida1, Yukihiro Tokumine1, Shinsaku Shimamoto2,

Hisashi Shimoyama2, Hideharu Ogiyama3, Syusaku Tsutsui3
1

市立伊丹病院 血液内科、2市立伊丹病院 循環器内科、3市立伊丹病院 消化器内科

Department of Hematology, Itami City Hospital, Hyogo, Japan, 2Department of Cardiology, Itami City Hospital, Hyogo, Japan,

1

Department of Gastroenterology, Itami City Hospital, Hyogo, Japan

3

125

ポスター９

A-59-years old female was admitted to our hospital because of heart failure, but the obvious cause of heart failure was
unknown. Later, we found the decrease of normal Ig, the presence of urinary BJ protein, the increase of bone marrowplasma cell count(8%). She was diagnosed as cardiac AL amyloidosis by myocardial biopsy. We aimed for carrying out
autologous peripheral blood stem cell transplant (ASCT), started BD therapy. But the sinus arrest developed on day8,
so a pacemaker was implanted. After that, she was bleeding in the third course of BD therapy Endoscopic examination
revealed a wide range of ulcers in the stomach. We failed endoscopic hemostasis due to the extensive hemorrhagic
lesions. We stopped anticoagulation therapy and repeated blood cell transfusions. Also in the biopsy of gastric mucosa,
amyloid deposition was confirmed. After that, we restarted BD therapy and developed treatment to CyBorD, but a highfever of unknown origin persisted two weeks. So, chemotherapy was discontinued again and heart failure had worsened.
We judged both stem cell harvest and ASCT to be impossible. It is planned to change to other new drugs such aslenalidomide in the future. [Discussion] Cardiac AL amyloidosis is known as a very poor prognostic disease. The caseswith improved cardiac function have been reported by treatment with new drugs based on myeloma and ASCT. However,in these cases, it is important to survive the early worsening of heart failure. In the treatment of cardiac amyloidosis,
cooperation with us and cardiologists and gastroenterologists is very important.

ポスター発表（Poster Presentation）

P9-5

Phase 3 Study of Cyclophosphamide/Bortezomib/Dexamethasone (CyBorD)±Daratumumab(DARA) in Newly Diagnosed Amyloid Light Chain Amyloidosis: ANDROMEDA

Raymond L. Comenzo1、Arnaud Jaccard2、Efstathios Kastritis3、Mathew Maurer4、Jeffrey Zonder5、Monique C. Minnema6、Stefan Schӧnland7、Ashutosh Wechalekar8、Xiang Qin9、Sandra Y. Vasey9、Imran Khan10、Jordan M. Schecter10、鈴木 晶子 11、辻村 涼 11、Giampaolo Merlini12

Raymond L. Comenzo1, Arnaud Jaccard2, Efstathios Kastritis3, Mathew Maurer4, Jeffrey Zonder5, Monique C. Minnema6,

Stefan Schӧnland7, Ashutosh Wechalekar8, Xiang Qin9, Sandra Y. Vasey9, Imran Khan10, Jordan M. Schecter10, Akiko Suzuki11,
Ryo Tsujimura11, Giampaolo Merlini12

1

Division of Hematology/Oncology, John C. Davis Myeloma and Amyloid Program, Tufts Medical Center, Boston, MA, 2CHU

Dupuytren, Limoges, France, 3Univ. of Athens School of Medicine, Alexandra General Hospital, Athens, Greece, 4Presbyterian

Hospital and Vanderbilt Clinic, New York, NY, 5Barbara Ann Karmanos Cancer Institute, Detroit, MI, 6UMC Utrecht, Utrecht,
Netherlands, 7Heidelberg Univ. Hospital, Heidelberg, Germany, 8Univ. College London and the Royal Free London NHSFoundation Trust, London, UK, 9Janssen Research & Development, LLC, Spring House, PA, USA, 10Janssen Research &Development, LLC, Raritan, NJ, USA, 11Janssen Pharmaceutical K.K., Tokyo, Japan, 12Scientific Institute Policlinico San Matteo,

University of Pavia, Italy

DARA, a human IgGκ mAb targeting CD38, is approved as monotherapy and in combination with standard of careagents for relapsed or refractory and newly diagnosed multiple myeloma (MM). DARA monotherapy demonstrated atolerable safety profile and encouraging hematologic responses in heavily treated amyloid light-chain (AL) amyloidosis.
Here, we describe the design of a phase 3 study of CyBorD±DARA in newly diagnosed AL amyloidosis. Following asafety run-in of CyBorD+DARA in ≥10 pts, ~360 pts will be randomized to CyBorD±DARA. Key eligibility criteria
include ≥18 y of age; measurable disease; ≥1 impacted organ; ECOG performance status of 0-2; absolute neutrophil
count ≥1.0×109/L; hemoglobin ≥8.0 g/dL; platelet count ≥50×109/L; eGFR ≥20 mL/min/1.73m2; NT-ProBNP ≤8,500 ng/L;and no prior AL amyloidosis or MM therapy. DARA 1,800 mg will be given SC QW in Cycles 1-2, Q2W in Cycles 3-6,
and Q4W until disease progression or subsequent therapy for ≤2 y. All pts will receive PO or IV Cy 300 mg/m2 and Bor(SC) 1.3 mg/m2 on Days 1, 8, 15, 22 of each 28-day cycle for ≤6 cycles. D 40 mg (PO or IV) will be given on Days 1, 8,
15, 22. D 20 mg will be given the day of DARA dosing and the day following dosing. Other pre and post DARA dosing
medications are as per label. The primary endpoint is overall complete hematologic response rate; secondary outcomes
include major organ deterioration PFS (MOD-PFS), PFS, organ response rate, overall survival, time and duration of
response, health-related quality of life, safety, pharmacokinetics, and MRD. ClinicalTrials.gov, NCT03201965.

126

ポスター発表（Poster Presentation）

P10-1
依田
竹村

多発性骨髄腫患者に対する自家移植後の地固め療法のリスクとベネフィット
Risks and benefits of consolidation therapy after autologous stem cell transplantation for
multiple myeloma

在理、永田 泰之、伊東兼成、小野 孝明侑治郎、高木文智、中野

洸太郎、内山

哲、坂本

奈美、高羽

理光、安達

美和、

Akari Yoda, Yasuyuki Nagata, Yujiro Ito, Fumisato Takagi, Kotaro Nakano, Satoshi Uchiyama, Nami Sakamoto,
Masamitsu Takaba, Miwa Adachi, Tomonari Takemura, Takaaki Ono

浜松医科大学医学部附属病院 血液内科

Division of Hematology, Hamamatsu University School of Medicine, Japan

ポスター９【Background】Consolidation and maintenance therapies for multiple myeloma (MM) after autologous stem celltransplantation (ASCT) have been reported to improve the treatment response rate. However, the role of consolidation
therapy has not been elucidated.
【Methods】We retrospectively evaluated the efficacy and safety of consolidation therapy in MM patients who underwent
ASCT from 2014 to 2017.
【Results】Thirteen patients (8 males; median age 56 years, range 42-69) were evaluated. Patients characteristics wereas follows: IgG, IgA, and BJP were 9, 2 and 2, respectively; 4, 8, and 1 patients had Revised ISS stage Ⅰ, Ⅱ, and Ⅲ,
respectively. Three patients received no treatment after ASCT. Seven received consolidation therapy (KLd, 4 ; BLd, 1 ;BD, 1 ; CBD, 1). Thirteen patients received maintenance therapy(Ld, 3 ; lenalidomide without dexamethasone, 3 ; ELd, 7).
The CR rate improved from 0% to 71.4% after consolidation therapy; VGPR rate improved from 14.2% to 85.7%. Grade
3/4 leukocytopenia and thrombocytopenia during consolidation therapy were observed in 85.7% and 42.9%, respectively.
Grade 3 hemorrhagic cystitis was seen in 14.3%. In contrast, hematological toxicities in patients who did not receive
consolidation were grade 2 or less during maintenance therapy.
【Conclusion】Consolidation therapy followed by maintenance therapy improved the treatment response rate obtained
after ASCT. However, consolidation therapy could not be continued in some patients due to toxicity. It is reasonable toconsider pre-ASCT treatment regimens without consolidation therapy.

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127

ポスター発表（Poster Presentation）

P10-2

移植適応多発性骨髄腫において初回自家末梢血幹細胞採取不良が予後に与える影響
The impact of poor PBSC mobilization on the outcome of patients with multiple myeloma

長井 友莉恵 1、三村 尚也 1,2、石井 改 1、一色 佑介 1、杉田 泰雅 3、大島竹田 勇輔 1、武内 正博 1、大和田 千桂子 1、井関 徹 1,2、深澤 元晴 4、原堺田 惠美子 1

渚 1、三川 紫緒 1,2、塚本 祥吉 1、
暁 5、趙 竜桓 6、中世古 知昭 1,7、Yurie Nagai1, Naoya Mimura1,2, Arata Ishii1, Yusuke Isshiki1, Yasumasa Sugita3, Nagisa Oshima1, Shio Mitsukawa1,2,

Shokichi Tsukamoto1, Yusuke Takeda1, Masahiro Takeuchi1, Chikako Ohwada1, Tohru Iseki1,2, Motoharu Fukazawa4,

Satoru Hara5, Ryuko Cho6, Chiaki Nakaseko1,7, Emiko Sakaida1
1

千葉大学医学部附属病院 血液内科、2千葉大学医学部附属病院 輸血・細胞療法部、3国保大網病院 血液内科、
JCHO船橋中央病院 内科、5千葉ろうさい病院 腫瘍血液内科、6千葉県済生会習志野病院 血液内科、
7
国際医療福祉大学医学部 血液内科
4

Department of Hematology, Chiba University Hospital, Japan, 2Department of Transfusion Medicine and Cell Therapy, Chiba

1

University Hospital, Japan, 3Department of Hematology, Oami Municipal Hospital, Japan, 4Department of Internal medicine,

JCHO Funabashi Central Hospital, Japan, 5Department of Hematological Oncology, Chiba Rosai Hospital, Japan, 6Department of
Hematology, Chibaken Saiseikai Narashino Hospital, Japan, 7Department of Hematology, International University of Health andWelfare School of Medicine, Japan

Background: Autologous stem cell transplantation (ASCT) is an important strategy to improve patient outcome inmultiple myeloma (MM). However, the impact of poor mobilization of peripheral blood stem cells (PBSCs) on theoutcome has not yet been clearly illustrated. Methods: Clinical characteristics and outcomes of 95 MM patients
who underwent PBSC harvest (PBSCH) at our institute between 2008 and 2018 were retrospectively analyzed. Poor
mobilizers were defined as patients with less than 2×106 /kg of CD34+cells harvested at the first mobilization. Results:
20 (21%) out of 95 patients were poor mobilizers. The median age at PBSCH was significantly higher in the poor
mobilizers than the others (64 vs 60 yrs, p<0.01). Among 90 patients who received following ASCT, the median countsof transplanted CD34+ cells were 1.62×106/kg in the poor mobilizers (n=17) and 2.43×106/kg in the others (n=73).
While there were no significant differences in the median days of neutrophil engraftment (12.5 vs 12.0, p=0.88), thoseof platelet engraftment were significantly longer in the poor group (16.0 vs 14.0, p=0.03). Median PFS and OS from thetransplantation were not significantly different (p=0.75, p=0.46). Importantly, three poor mobilizers could not receive
ASCT. Conclusion: The prognosis of poor mobilizers who could undergo ASCT was similar to that of the others inour study. Since it is still unclear whether poor mobilizers who cannot receive ASCT have poor outcome or not, further
investigations in larger cohorts are needed.

128ポスター発表（Poster Presentation）

P10-3
塚田
鈴木

信弘、梨本
憲史

当院で行った再発・難治多発性骨髄腫に対する非血縁者間骨髄移植 14 例の検討
Unrelated bone marrow transplantation for relapsed/refractory multiple myeloma
淳一郎、宇藤

唯、佐藤

広太、宮崎

寛至、小倉

瑞生、吉識

由実子、阿部有、石田禎夫、Nobuhiro Tsukada, Junichiro Nashimoto, Yui Uto, Kota Sato, Kanji Miyazaki, Mizuki Ogura, Yumiko Yoshiki, Yu Abe,
Tadao Ishida, Kenshi Suzuki

日本赤十字社医療センター 血液内科

Department of Hematology, Japanese Red Cross Medical Center, Japan[Background]
Allogeneic SCT is one of treatment option for patients with multiple myeloma (MM) refractory to novel agents. It is
an important issue to argue appropriate conditioning regimens and stem-cell sources, and patient population who will
benefit from allo-SCT.
[Methods]
We retrospectively analyzed 14 consecutive patients who received unrelated BMT (uBMT) for relapsed and refractory
MM between Jul 2012 and Nov 2018 at Japanese Red Cross Medical Center. Characteristics of patients, PFS, and OS
were analyzed.
[Results]
Median age at uBMT was 47 (range 31-61) and M:F=4:10. Five patients received BMT from HLA 8/8 matched unrelateddonor (MUD) and 9 patients received BMT from HLA mismatched unrelated donor (MMUD). All 14 patients received
conditioning regimen including 8Gy of TBI. Responses before uBMT were CR: 3, VGPR: 6, PR: 2, SD: 3. Five-year
PFS was 46% (95%CI: 13-75) and 5-year OS was 57% (95%CI: 20-82). Four patients died during observation period
and causes of death were primary disease: 3 and TRM: 1. Recipients of MMUD showed significantly better PFS (p=0.015)
and OS (p=0.014). Among 10 patients surviving, 4 patients received treatments including maintenance therapy.
[Conclusions]
It is interesting that recipients of MMUD showed better PFS, suggesting graft-versus-myeloma effects. MMUD can bechosen if matched related or HLA 8/8 matched unrelated donors are not immediately available. Allo-SCT from unrelateddonors can be an effective treatment option if patients and donors are appropriately selected.
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10

129

ポスター発表（Poster Presentation）

P10-4
岡塚
阿部

移植適応の初発多発性骨髄腫に対する modified RVD-lite の有効性と安全性に関する後方視的解析
Retrospective analysis of the efficacy and safety of modified bortezomib-lenalidomidedexamethasone litefor transplant eligible NDMM

貴世志、石田 禎夫、余語 孝夫、梨本有、塚田 信弘、鈴木 憲史

淳一郎、宇藤

唯、佐藤

広太、宮崎

寛至、小倉

瑞生、吉識

由実子、

Kiyoshi Okazuka, Tadao Ishida, Takao Yogo, Junichiro Nashimoto, Yui Uto, Kota Sato, Kanji Miyazaki, Mizuki Ogura,
Yumiko Yoshiki, Yu Abe, Nobuhiro Tsukada, Kenshi Suzuki

日本赤十字社医療センター 血液内科

Department of Hematology, Japanese Red Cross Medical Center, Japan[Background]TheRVDfor newly diagnosed multiple myeloma has been one of the standard induction therapies.
However, 9-23 % of discontinuation rate was reported. Here, we investigated the efficacy and safety of modified RVDlite(mRVD-lite) for 46 transplant eligible patients with NDMM. [Patients]We retrospectively analyzed 46 transplanteligible NDMM. Bortezomib and oral dexamethasone were administered on days 1, 8, 15, 22. Lenalidomide 15 mg/
day was given on days 2-7, 9-14, 16-21. [Results]The ORR after four 28-day cycles of mRVD-litewas obtained in 40(87.0%), including sCR in 6 (13.0%) and CR in 5 (10.9%). SD and PD were observed in 3 patients (6.5%) and 1 patient(2.2%), respectively. Thirty-seven of 46 patients (80.4%) received autologous stem cell transplantation (ASCT) afterat least 4 courses of mRVD-lite. Response after ASCT were sCR in 17(44.7%), CR in 3 (7.9%), VGPR in 8 (21.2%)
and PR in 9 (23.7%). Grade 3 or higher adverse events (AEs) were observed in 17 (37.8%). Only one patient (2.2 %)discontinuedmRVD-litebecause of grade 3 peripheral neuropathy.[Conclusions]The ORR after 4 cycles ofmRVD-litewas
high (91.1%). These results might be related to low rate of discontinuation of treatment. Also, the ORR after ASCT wascomparable to the results previously published. AEs in mRVD-litewere feasible and manageable in most patients. Our
results suggest that mRVD-liteis very feasible and effective treatment for patients with transplant eligible NDMM.

130

ポスター発表（Poster Presentation）

P10-5
宮崎

寛至、石田

メルファランを前処置とした自家造血幹細胞移植症例における食事調整による経口摂取と早期経静脈栄養の比較
Early Parental Nutrition Versus Food Modification in Patients Undergoing Autologous
Transplantation
禎夫、鈴木

憲史

Kanji Miyazaki, Tadao Ishida, Kenshi Suzuki

日本赤十字社医療センター 血液内科

Department of Hematology, Japanese Red Cross Medical Center, Japan

Introduction: Autologous hematopoietic cell transplantation is one of the most effective therapies for patients withplasma cell dyscrasias. This study aimed to compare the duration of hospital stay and complications of parental nutrition
and food modification in patients undergoing autologous transplantation.
Methods: We retrospectively reviewed medical records of 172 patients with multiple myeloma or AL amyloidosis who
underwent autologous transplantation at our institution. The primary outcome was the duration of hospital stay from theday of transplantation.
Results: Of the 172 study patients, 104 had multiple myeloma and 68 had AL amyloidosis. Early parental nutrition
was administered in 104 (60.5%) patients. The median duration of hospital stay was significantly longer in the parental
nutrition group than in the non-parental nutrition group (median, 23 days versus 20 days, p = 0.012). After excluding
patients who could eat more than 800 kcal a day, 68.6% (96/140) of patients were administered parental nutrition and31.4% (44/140) of patients received food modification by dieticians; of these patients, only 2 received enteral nutrition,and the median duration of hospitalization was significantly longer in the parental nutrition group than in the foodmodification group (median, 23 days versus 19 days, p = 0.036). Upon multivariate analysis, parental nutrition was
identified as an independent risk factor (HR 1.561, 95%CI 1.075–2.267, p = 0.019).
Conclusions: Parental nutrition in patients undergoing autologous transplantation is associated with extended hospital
stay.

ポスター
10

131

ポスター発表（Poster Presentation）

P11-1
小山

大輔、伊藤

自家移植適応の初発高リスク多発性骨髄腫に対するカルフィルゾミブ・レナリドミド・デキ
サメサゾンによる寛解導入療法
Carfilzomib with lenalidomide and dexamethasone prior to high-dose therapy for newly
diagnosed high-risk multiple myeloma
理恵、山本

里美、井本

直人、倉橋

信悟、杉浦

勇

Daisuke Koyama, Rie Ito, Satomi Yamamoto, Naoto Imoto, Shingo Kurahashi, Isamu Sugiura

豊橋市民病院 血液・腫瘍内科

Devision of Hematology and Oncology, Toyohashi Municipal Hospital, Japan[Introduction] The prognosis of patients with high-risk multiple myeloma (HRMM) is still poor even in the eraof novel agents. Carfilzomib (CFZ/K), the 2nd generation proteasome inhibitor, is effective even in relapsed MM
irrespective of cytogenetic risk. Here, we investigated the feasibility of CFZ, lenalidomide (LEN/R) and dexamethasone(Dex) combination (KRd) in patients with newly diagnosed, transplant-eligible HRMM. [Patients and method] We
retrospectively reviewed the medical records of 5 patients with transplant-eligible HRMM newly diagnosed between Apr.
2017 and Dec. 2018. All patients received one cycle of bortezomib (B), LEN and Dex induction while the cytogenetic
analysis was performed. After confirming HR cytogenetic abnormalities (CA), 2 or 3 cycles of KRd were given prior to
HDT. As a consolidation and maintenance, 3 cycles of KRd and then Bd or Rd were given. [Results] The median age
was 65 years. Detected CA were complex karyotype in all patients, t(4;14) in 2 patients, and del(17p) in one patient. In
2 patients, planned KRd was substituted by Kd due to renal insufficiency and grade 3 rash. Two patients discontinued
KRd/Kd due to progressive disease and grade 4 acute heart failure. All 3 patients who completed KRd/Kd underwent
HDT/ASCT, and they all achieved sCR. [Discussion] KRd therapy was tolerable in most patients. However, one patient
experienced sudden cardiac failure with quick recovery. With close monitoring of cardiovascular events, KRd canprovide an excellent treatment response. Prospective study in larger cohort should be warranted.

132ポスター発表（Poster Presentation）

P11-2

当院における多発性骨髄腫に対する強度減弱前処置による同種造血幹細胞移植の後方視的解析
Retrospective analysis of reduced intensity conditioning allogeneic hematopoietic
transplantation for multiple myeloma at Chiba university hospital

武内 正博 1、田波 貴彬 1、畑中 康人 1、柴宮 明日香 1、石井 改 1、長井 友莉恵 1、三科 達三 1、山﨑 美貴 1、
一色 佑介 1、栢森 健介 1、木村 賢司 1、高石 浩司 1、日野 裕太郎 1、塚本 祥吉 1、三川 紫緒 1,2、竹田 勇輔 1、
三村 尚也 1,2、大和田 千桂子 1、井関 徹 1,2、中世古 知昭 1,3、堺田 惠美子 1
Masahiro Takeuchi1, Takaaki Tanami1, Yasuhito Hatanaka1, Asuka Shibamiya1, Arata Ishii1, Yurie Nagai1, Tatsuzo Mishina1,
Miki Yamazaki1, Yusuke Isshiki1, Kensuke Kayamori1, Kenji Kimura1, Koji Takaishi1, Yutaro Hino1, Shokichi Tsukamoto1,

Shio Mitsukawa1,2, Yusuke Takeda1, Naoya Mimura1,2, Chikako Ohwada1, Tohru Iseki1,2, Chiaki Nakaseko1,3, Emiko Sakaida1

1

千葉大学医学部附属病院 血液内科、2千葉大学医学部附属病院 輸血・細胞療法部、3国際医療福祉大学医学部 血液内科

Department of Hematology, Chiba University Hospital, Japan, 2Department of Transfusion Medicine and Cell Therapy, Chiba

1

University Hospital, Japan, 3Department of Hematology, International University of Health and Welfare School of Medicine,Japan【Background】
Despite recent treatment advances, multiple myeloma (MM) remains an incurable disease. Allogeneic hematopoietic
stem cell transplantation (HSCT) is not considered as a standard of care due to high treatment-related mortality. To
reduce treatment-related mortality, we performed reduced-intensity conditioning allogeneic HSCT for relapsed or
refractory MM.
【Patients and Methods】We performed a retrospective review of 16 patients in the database from 2000 to 2018 who
underwent allogeneic HSCT for myeloma at Chiba university hospital.
【Results】Median follow-up period was 1173 days (range 160 – 5570). Median age at transplant was 49.5 years (range
24 – 61). All patients underwent autologous HSCT before allogeneic HSCT and received reduced-intensity conditioning.
Twelve patients underwent related peripheral blood stem cell transplant (matched 11, haplo-identical 1), four patients
underwent unrelated bone marrow transplant. Treatment-related mortality was 0% at day 100. Acute and chronic graft
versus host disease developed in 81% and 75% patients, respectively. Two year and five-year overall survival rates were
67% and 44% respectively. The major cause of death was disease progression (7 out of 10 deaths). Of note, two patientsremain CR for more than ten years after transplant.
【Conclusion】Reduced-intensity conditioning allogeneic HSCT for MM is one of the options for relapsed or refractory
myeloma patients and have the potential to cure MM.

ポスター
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133

ポスター発表（Poster Presentation）

P11-3
倉橋

CyBorD 寛解導入療法を用いた初発多発性骨髄腫に対する自己末梢血幹細胞移植の長期成績
Long-term outcome of CyBorD induction and autologous peripheral blood stem celltransplantation for patients with newly diagnosed multiple myeloma

信悟 1、奥野真吾 1,2、伊藤理恵 1、山本里美 1、小山大輔 1、井本直人 1、杉浦勇1

Shingo Kurahashi1, Shingo Okuno1,2, Rie Ito1, Satomi Yamamoto1, Daisuke Koyama1, Naoto Imoto1, Isamu Sugiura1
1

豊橋市民病院 血液・腫瘍内科、2名古屋大学大学院医学系研究科 血液・腫瘍内科学

Division of Hematology and Oncology, Toyohashi Municipal Hospital, Japan, 2Department of Hematology and Oncology,

1

Nagoya University Graduate School of Medicine, Japan

To investigate the long-term outcome of CyBorD (CPA, BOR, DEX) induction prior to auto-PBSCT for patients (pts)with newly diagnosed multiple myeloma comparing with CVAD (CPA, VCR, ADR, DEX) induction, we retrospectively
reviewed the medical records of 70 pts transplanted from Aug. 2000 to Jan. 2017 in Toyohashi Municipal Hospital.
Overall 34 pts and 36 pts were treated CyBorD and CVAD, respectively. The median age was 60(38-68) years. As for
R-ISS, stage Ⅲ was 16(47.0%) in CyBorD group, and 15(41.7%) in CVAD group. The treatment response before autoPBSCT was sCR/CR(5.8%), VGPR(38.2%) in CyBorD group, and sCR/CR(5.6%), VGPR(8.3%) in CVAD group,
respectively. The median follow-up was 94.9 months (mo.). The median relapse-free survival (RFS) from auto-PBSCT
was 34.2 mo. in CyBorD group, and 15.6 mo. in CVAD group. Pts in CyBorD group showed a longer RFS, but notstatistically significant (p=0.1532). The median overall survival (OS) was 70.7 mo. in CyBorD group, and 106.1 mo. in
C-VAD group. There were no significant differences in RFS between two groups in pts with R-ISS stage Ⅲ . Pts withhigh LDH had poor RFS in both groups (3.0 mo. in CBD group, 11.0 mo. in CVAD group). Pts with del17p also had poor
RFS in both groups (10.4 mo. in CBD group, 15.0 mo. in CVAD group). But, pts with t(4;14) had better RFS in CyBorD
group, significantly (61.5 vs 4.3 mo., p=0.0053). CyBorD was effective induction therapy especially for pts with t(4;14),
but pts with high LDH, del17p had poor prognosis, so further intervention might beneficial to such pts.

134

ポスター発表（Poster Presentation）

P11-4
吉原

享子、吉原

移植適応多発性骨髄腫患者に対する６サイクルの寛解導入療法（VRd/KRd）の安全性と有効性の検討
Feasibility of 6 cycles of VRd/KRd as an induction therapy prior to stem-cell collection intransplant-eligible multiple myeloma
哲、玉置

広哉、岡田

昌也、藤盛

好啓

Kyoko Yoshihara, Satoshi Yoshihara, Hiroya Tamaki, Masaya Okada, Yoshihiro Fujimori

兵庫医科大学病院 血液内科

Division of Hematology, Department of Internal Medicine, Hyogo College of Medicine, Japan

Previous studies have suggested that the achievement of VGPR
or CR with induction therapy has a major impact on the outcomes following SCT.
Although the longer and intensified induction therapy may provide a better disease
control, longer exposure to lenalidomide may negatively affect the stem-cellyield.
We conducted a prospective study, examining the feasibilityof the 6 courses of triplet-induction therapy prior to stem-cell collection.
Patients received modified VRd every 4 weeks for 6 courses. For the patients
who did not achieve VGPR after 3 courses of modified VRd, KRd was used in thelast two (4th and 5th) courses. Stem cell mobilization
was performed after cyclophosphamide (2g/m2) and G-CSF; the use ofplerixafor was reserved as a second PBSCH attempt.
Eleven patients were enrolled to the study. Two patients
dropped out due to adverse events and one patient has not completed theinduction therapy. Among 8 evaluable patients (median age, 68 years old [45-70]), 4
patients were switched from VRd to KRd according to the above mentioned
protocol. Seven out of 8 patients achieved VGPR or CR after the completion of theinduction therapy. The first stem cell collection in all of the patients provided
the minimal acceptable stem cell yield, defined as ≥2 × 106 CD34+
cells/kg (median 3.5 x 106 CD34+ cells/kg [2.0-6.7]). They underwent
stem cell transplantation following high-dose melphalan, and achieved neutrophil
and platelet engraftment.
ポスター

Our observation support 6 cycles of VRd/KRd as anefficacious and safe induction strategy prior to stem-cell collection.

11

135

ポスター発表（Poster Presentation）

P12-1
碓井

日本における多発性骨髄腫への新規薬剤導入の影響：罹患率と死亡率の経年変化の評価
The impact of novel agents on multiple myeloma: trend of incidence and mortality in Japan

喜明 1,4、伊藤

秀美 1、小栁友理子 1、松田

智大 2、片野田耕太 3、前田嘉信 4、松尾恵太郎 5

Yoshiaki Usui , Hidemi Ito , Yuriko Koyanagi , Tomohiro Matsuda , Kota Katanoda , Yoshinobu Maeda , Keitaro Matsuo5
1,4

1

1

2

3

4

1

愛知県がんセンター研究所 がん予防医療研究領域 がん情報・対策研究分野、
国立がん研究センター がん情報対策センター がん登録センター、3国立がん研究センター がん情報対策センター がん統計・総合解析研究部、4岡山大学大学院 医歯薬総合研究科 血液・腫瘍・呼吸器内科学、
5
愛知県がんセンター研究所 がん予防医療研究領域 がん予防研究分野
2

Division of Cancer Information and Control, Department of Preventive Medicine, Aichi Cancer Center Research Institute, Aichi,

1

Japan, 2Division of Cancer Registries Integration, Center for Cancer Control and Information Services, National Cancer Center,

Tokyo, Japan, 3Division of Cancer Statistics Integration, Center for Cancer Control and Information Services, National Cancer

Center, Tokyo, Japan, 4Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate Schoolof Medicine, Dentistry and Pharmaceuticals Sciences, Okayama, Japan, 5Division of Cancer Epidemiology and Prevention,
Department of Preventive Medicine, Aichi Cancer Center Research Institute, Aichi, Japan

Background;
Treatment for multiple myeloma (MM) has dramatically changed in the past two decades thanks to novel agents.
Although improvement in survival rate has been shown in several clinical trials, the impact of novel agents on mortality
has not been adequately evaluated. To evaluate the impact of novel agents on the public health, we observed trend in
mortality of MM in Japan, considering the effect of trend in incidence.
Patients and method;
We used incidence data from population-based cancer registries and mortality data from national statistics in Japan. The
period covered in this analysis is 1995-2015, during which 74,972 patients in Japan died from MM. We used joinpoint
regression analysis to characterize trends in the age-standardized rate (ASR) of incidence and mortality of MM. Stratified
analysis by age was also performed.
Result;Although the ASR of incidence has a trend of increasing, the ASR of mortality decreased significantly after theavailability of novel agents. The change in the trend occurred in 2004. After stable trend, the ASR of mortality decreased
with annual percent change (APC) of 2.4% (95% CI 2.1-2.8%). Especially, among people aged 70-79 years, the mortality
rate decreased with APC of 3.2% (2.7-3.7%) from 2004 to 2015, after increasing with APC of 1.2% (0.4-2.1%). The
period of change in mortality trend seems to associate with the period in which the novel agents appeared.
Conclusion;
We observed the improvement of mortality rate of MM in novel agents’ era, especially for the elderly who had notreceived benefit from conventional chemotherapy.

136

ポスター発表（Poster Presentation）

P12-2

日常診療における多発性骨髄腫の治療成績とそれに及ぼす予後因子の検討
Real-world patient characteristics and outcomes of multiple myeloma

秋月 渓一 1、松岡 均 2、外山
河野 浩 2、武内 正紀 2、関根久冨木 庸子 1、下田 和哉 1

孝典 3、石崎 淳三 4、山下 清 5、河野 徳明 5、前田 宏一 6、佐藤 誠一 7、
雅明 1、上運天 綾子 1、田平 優貴 1、亀田 拓郎 1、幣 光太郎 1、日髙 智徳 1、Keiichi Akizuki1, Hitoshi Matsuoka2, Takanori Toyama3, Junzou Ishizaki4, Kiyoshi Yamashita5, Noriaki Kawano5,

Kouichi Maeda6, Seiichi Satou7, Hiroshi Kawano2, Masaki Takeuchi2, Masaaki Sekine1, Ayako Kamiunten1, Yuuki Tahira1,
Takurou Kameda1, Koutarou Shide1, Tomonori Hidaka1, Youko Kubuki1, Kazuya Shimoda1

1

宮崎大学医学部付属病院 内科学講座消化器血液学分野、2古賀総合病院、3宮崎県立延岡病院、4愛泉会日南病院、
宮崎県立宮崎病院、6国立病院機構 都城医療センター、7医療法人啓仁会 城南病院

5

Gastroenterology and Hematology, Dept.Int.Med., Miyazaki Univ, Japan, 2KOGA GENERAL HOSPITAL, Japan, 3Miyazaki

1

Prefectural Nobeoka Hospital, Japan, 4Aisenkai Nichinan Hospital, Japan, 5Miyazaki Prefectural Miyazaki Hospital, Japan,
Miyakonojo Medical Center, Japan, 7Jonan Hospital, Japan6

The prognosis of patients with multiple myeloma (MM) is improving. We surveyed the real-world data of 286 patients
who were newly diagnosed with MM between 2010 and 2018 in Miyazaki Prefecture. The median age at diagnosis
was 71 years (68% of patients were aged ≥65 years). The International Staging System (ISS) stage at diagnosis was I in
16.4% of patients, II in 30.8%, and III in 42.7%. As an initial therapy, 37 patients (12.9%) were treated with bortezomib+ lenalidomide + dexamethasone, 141 (49.3%) with bortezomib-based regimens, 26 (9.1%) with lenalidomide-based
regimens, 17 (6.0%) with thalidomide-based regimens, and 65 (22.7%) with conventional chemotherapy. In total, 80% of
patients were treated with one or more novel agents. Autologous stem cell transplantation (auto-SCT) was performed in
47 patients (16.4%). The median follow-up period was 25.0 months. The overall response rate (partial response (PR) or
better) to the initial therapy was 84.3%. The median survival time after diagnosis was 50.6 months, and the 3-year overall
survival (OS) was 60.8%. In univariate analysis, age ≤65 years, ISS stage I/II, use of novel agents as initial therapy, autoSCT, and superior response to initial treatment (PR or better) were associated with favorable prognosis. In multivariate
analysis, ISS stage I/II and superior response to initial treatment were identified as independent prognostic factors. Since
the 3-year OS in ISS III patients with a poor response to initial therapy was only 22.5%, early changes to therapeuticstrategies might be warranted.

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ポスター発表（Poster Presentation）

P12-3
寺尾
末永

俊紀、北館
孝生

多発性骨髄腫における長期生存症例の臨床的特徴
Long-term multiple myeloma survivors; clinical features of patients who survived longer
than 10-years
明宏、安部

佳亮、津島

隆史、小林

宏紀、三浦

大典、成田

健太郎、竹内正美、Toshiki Terao, Akihiro Kitadate, Yoshiaki Abe, Takafumi Tsushima, Hiroki Kobayashi, Daisuke Miura, Kentaro Narita,
Masami Takeuchi, Kosei Matsue

亀田総合病院

Kameda Medical Center, Japan

Background: This study aimed to investigate the clinical characteristics of long-term survivors with multiple myeloma(MM) in the novel agent era.
Methods: We retrospectively identified 182 consecutive patients with symptomatic MM who were diagnosed before
2009 and treated with novel agents at our institution.
Results: Among the all patients, 22 (12.1%) patients showed their overall survival longer than 10 years (long-term
survivors). Most of these survivors (91%) received novel agents. These patients were significantly younger (median, 67
vs. 72 years, p=0.007) and showed higher complete remission (CR) rate (50% vs. 6.8%, p<0.001) than the remaining
patients, whereas there was no significant inter-group difference in immunoglobulin subtypes and disease stages
including the International Staging System and Durie-Salmon stages. Among the long-term survivors, no patient carriedhigh-risk cytogenetic abnormality t(4;14), t(14;16), or del(17p). Additionally, 5 (22.7%) patients achieved only partial
response (PR) as a best response and 14.3% of the patients achieved minimal residual disease (MRD) levels of <1.0×10-4.
Conclusions: Our findings suggest that baseline youthfulness in long-term survivors might allow them to tolerate more
intensive and continuous treatment with novel agents. Relatively high proportion of patients who achieved only PR andhigher MRD levels indicates that not only the temporal depth of response, but also longitudinal therapeutic approaches
might be beneficial in terms of long-term survival.

138

ポスター発表（Poster Presentation）㊝ P12-4

多発性骨髄腫患者における PIM2, TAK1 の重要性
PIM2 and phosphorylated TAK1 expression as important prognostic factors in patients withmultiple myeloma

中村 信元 1、三木 浩和 2、寺町 順平 3、天真 寬文 4、日浅 雅博 5、小田 明日香 1、岡本 恵暢 1、大浦 雅博 1、
曽我部 公子 1、高橋 真美子 1、岩佐 昌美 1、宇高 憲吾 1、原田 武志 1、藤井 志朗 1、賀川 久美子 1、
安倍 正博 1
Shingen Nakamura1, Hirokazu Miki2, Jumpei Teramachi3, Hirofumi Tenshin4, Masahiro Hiasa5, Asuka Oda1,

Yasunobu Okamoto1, Masahiro Oura1, Kimiko Sogabe1, Mamiko Takahashi1, Masami Iwasa1, Kengo Udaka1, Takeshi Harada1,
Shiro Fujii1, Kumiko Kagawa1, Masahiro Abe1

1

徳島大学大学院医歯薬学研究部血液・内分泌代謝内科学、2徳島大学病院輸血・細胞治療部、
徳島大学大学院医歯薬学研究部口腔組織学分野、4徳島大学大学院医歯薬学研究部口腔顎顔面矯正学、
5
徳島大学大学院医歯薬学研究部生体材料工学分野
3

Department of Hematology, Endocrinology and Metabolism, Institute of Biomedical Sciences, Tokushima University Graduate

1

School, Tokushima, Japan, 2Department of Transfusion Medicine and Cell Therapy, Tokushima University hospital, Tokushima,

Japan, 3Department of Histology and Oral Histology, Tokushima University, Tokushima, Japan, 4Department of Orthodontics
and Dentofacial Orthopedics, Tokushima University, Tokushima, Japan, 5Department of Biomaterials and Bioengineering,

Tokushima University, Tokushima, Japan

We have demonstrated that PIM2 and TAK1 are important mediators in multiple myeloma (MM) microenvironment.
We aimed to investigate the association between clinical information and immunohistochemical expression of PIM2
and phosphorylated TAK1 (pTAK1) in bone marrow samples of MM patients. This study was approved by the internal
review board of the Tokushima University (permission number 2638-3).Fifty samples derived from thirty patients who
were diagnosed with symptomatic MM after new drug era were enrolled. Mean participant age was 64.9±8.4 years (median66) with 13 males and 17 females. Twenty-five patients were diagnosed as Durie and Salmon Stage Ⅲ and seven patientswith ISS Stage Ⅲ . Immunohistochemical evaluation was performed with scoring by both of staining intensity and extent
of positively stained cells among CD138 positive tumor cells. Overall survival was not correlated with age, sex, stage
and history of stem cell transplantation. PIM2 expression level was a significantly adverse prognostic factor (high vslow: 50 vs 82 months, hazard ratio 2.62, p<0.05). pTAK1 expression was also adverse prognostic factor (positive vs null:
68.6 vs 102 months survival). High expression group of both of PIM2 and pTAK1 had poor survival compared to the low
expression group (high vs low:40.9 vs 81.8 months). The fraction of PIM2 positive cells were increased at the time of
relapse in four patients out of seven compared with that in the onset of MM. Therefore, PIM2 and TAK1 are important
prognostic factors in MM patients and development of novel drugs targeting them is required.

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139

ポスター発表（Poster Presentation）

P12-5
麻奥

SMM の後方視的検討：High risk SMM の抽出と早期治療の是非
Retrospective study of SMM : extraction of high risk SMM and early treatment

英毅 1、板垣充弘 1、片山雄太 1、岡谷健史 1、今中亮太 1、許鴻平 1、勝谷慎也 2、岩戸康治 2

Hideki Asaoku , Mitsuhiro Itagaki , Yuta Katayama , Takeshi Okatani , Ryouta Imanaka , Kouhei Kyo , Shinya Katsutani2,
1

1

1

1

1

1

Kouji Iwato2

1

広島赤十字・原爆病院 血液内科、2広島赤十字・原爆病院 検査部

Department of Hematology, Hiroshima Red cross Hospital & Atomic-bomb Survivors Hospital, Japan, 2Department of Clinical1

Laboratory, Hiroshima Red Cross Hospital & Atomic-bomb Survivors Hospital, Japan

Objective : To examine the risk factors of progression and the effect of early treatment in Smoldering multiple myeloma(SMM). Patients and methods: IgG and IgA type SMM 98 cases from 1990 to 2017 were retrospectively analyzed.
Results: 60 females, 38 men, aged 39 to 93 years old, average 70.2 years old. IgG type 83 cases, IgA type 15 cases. 18
cases were treated immediately after diagnosis. (Chemotherapy group : CTxG) 80 cases were watch and wait (Watch
group : WG) and 53/80 cases were followed for treatment. The 5 year non-treatment survival rate in patients with WG
is 31%. The 5 year overall survival rate was 73%. Analysis of the risk factor of progression was a significant risk factor
in the bone marrow plasma cell ratio of 15% or more and B2MG of 2.5 mg / L or more in univariate analysis, but also
in multivariate analysis with other factors added, these two factors It was extracted as an independent risk factor. Six of
7 cases who had these two factors (High risk SMM) required treatment within one year. Among 18 CTxGs, 15/18 was
more than 15% of bone marrow plasma cell ratio and 8/12 was B2MG 2.5 mg / L or more. There is no difference in
OS after treatment in CTxG and WG. Treatments in CTxG are regimens containing melphalan. In these treatments, theadvantage of early treatment was not observed in High risk SMM. Conclusion : As risk factors of progression in SMM,
the bone marrow plasma cell ratio 15%, B2MG 2.5 mg / L were extracted. We did not recognize the advantage of early
treatment for high risk SMM.

140

ポスター発表（Poster Presentation）

P13-1

当科での Daratumumab 5 例の使用経験
Experience with the Use of Daratumumab in Five Patients at Our Department

関口 康宣 1、飯塚 弘子 1、瀧澤 春子 1、若林 睦 1、杉元 啓二 1、坂尻
大久保 光夫 3、中村 紀子 4、澤田 朝寛 4、小松 則夫 5、野口 雅章 1

さくら 1、冨田

茂樹 2、泉

浩 2、

Yasunobu Sekiguchi1, Hiroko Iizuka1, Haruko Takizawa1, Mutsumi Wakabayashi1, Keiji Sugimoto1, Sakura Sakajiri1,

Shigeki Tomita2, Hiroshi Izumi2, Mitsuo Okubo3, Noriko Nakamura4, Tomohiro Sawada4, Norio Komatsu5, Masaaki Noguchi1
1

順天堂大学医学部附属浦安病院 血液内科、2順天堂大学医学部附属浦安病院 病理部、順天堂大学医学部附属浦安病院 輸血学研究室、4順天堂大学医学部附属浦安病院 臨床検査医学科、
5
順天堂大学医学部附属順天堂医院 血液内科

3

Department of Hematology, Juntendo University Urayasu Hospital, Japan, 2Department of Pathology, Juntendo University

1

Urayasu Hospital, Japan, 3Blood Transfusion Research Laboratory, Juntendo University Urayasu Hospital, Japan, 4Department ofLaboratory Medicine, Juntendo University Urayasu Hospital, Japan, 5Department of Hematology, Juntendo University Juntendo
Hospital, Japan[Objective] To verify problems regarding the efficacy, safety of daratumumab (Dara).
[Subjects and Methods] Data from 5 pts who had received Dara were analyzed retrospectively.
[Results] 4 men and 1 woman with a median age of 53 years (range: 48-71), 3 had received DVd and 2 had received
DRd. IgG in 2, BJP in 2 (including 1 with plasmacytoma(PC) and 1 with pleural effusion(PE)), and IgA in 1. Stage II
in 2 and Stage III in 3. Chromosomal changes were: no abnormality in 1, del 13q in 4, t(11;14) in 2, t(4;14) in 1, del 17p
in 1, and 1q21 in 1. The median number of prior therapy regimens was 5 (range: 2-10), and the median duration fromdiagnosis was 2.92 years (range: 0.67-7.5). The median number of cycles was 3 (range: 1-4). The best response was PR
in 3, SD in 1, and PD in 1. The final response was PR in 1, and PD in 4. The outcome was survival in 1 and death in 4.
AE that were encountered were cytopenia in 1, numbness in 1, infusion reaction in 1 and no in 3.
[Discussion] As the best response, PR was achieved in 3 and SD in 1; however, only 1 that the PR could be maintained
final response, while the final response was PD in 4. The Dara was undertaken at a late phase. The median number ofcycles was as small as 3. All AE were mild. Late phase could explain the failure to ensure long-term maintained response.
Dara afforded response against t(4;14), there was no response of the PC or PE. The efficacy of Dara in reversing the
prognostically unfavorable chromosomal aberration may suggest that the prognosis could be improved if Dara were usedduring the early phase.

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141

ポスター発表（Poster Presentation）

P13-2

当科での Elotuzumab 9 例の使用経験
Experience with the Use of Elotuzumab in Nine Patients at Our Department

瀧澤 春子 1、関口 康宣 1、飯塚 弘子 1、若林 睦 1、杉元 啓二 1、坂尻
大久保 光夫 3、中村 紀子 4、澤田 朝寛 4、小松 則夫 5、野口 雅章 1

さくら 1、冨田

茂樹 2、泉浩 2、Haruko Takizawa1, Yasunobu Sekiguchi1, Hiroko Iizuka1, Mutsumi Wakabayashi1, Keiji Sugimoto1, Sakura Sakajiri1,

Shigeki Tomita2, Hiroshi Izumi2, Mitsuo Okubo3, Noriko Nakamura4, Tomohiro Sawada4, Norio Komatsu5, Masaaki Noguchi1
1

順天堂大学医学部附属浦安病院 血液内科、2順天堂大学医学部附属浦安病院 病理部、順天堂大学医学部附属浦安病院 輸血学研究室、4順天堂大学医学部附属浦安病院 臨床検査医学科、
5
順天堂大学医学部附属順天堂医院 血液内科
3

Department of Hematology, Juntendo University Urayasu Hospital, Japan, 2Department of Pathology, Juntendo University

1

Urayasu Hospital, Japan, 3Blood Transfusion Research Laboratory, Juntendo University Urayasu Hospital, Japan, 4Department ofLaboratory Medicine, Juntendo University Urayasu Hospital, Japan, 5Department of Hematology, Juntendo University Juntendo
Hospital, Japan[Objective] To verify problems regarding the efficacy, safety of elotuzumab (Elo).
[Subjects and Methods] Data from 9 pts who had received Elo were analyzed retrospectively.
[Results] 4 male and 5 female with a median age of 67 years (range: 48-78), IgG in 4, BJP in 3, and IgA in 2. Stage II in
5 and Stage III in 4. High-risk chromosomal aberrations were in 4, non-high-risk in 3, and unknown in 2. The median
number of prior therapy regimens was 4 (range: 1-5), and the median interval from diagnosis was 4.9 years (range: 1.38.6). The median number of cycles of Elo was 4 (range: 1-16). The best response was PR in 3, SD in 3, and PD in 3.
The outcome was survival in 3 and death in 6. AE encountered were cytopenia in 5, sepsis in 1, and gastrointestinal
haemorrhage in 1; no in 2.
[Discussion] There were 6 in whom the best response was SD or better. Long-term Elo was accomplished in 2 (16cycles in 1 and 25 cycles in 1), and 2 with SD received relatively long-term Elo (4 cycles in 1 and 5 cycles in 1). As
for AE, gastrointestinal haemorrhage necessitated discontinuation of the therapy in 1 and sepsis resulted in death in 1.
Mild cytopenia was developed in 5. Elo is generally thought to be associated with infrequent AE, but caution should
be exercised, because serious AE could occur, as in the case included in this report. The present results also suggestthat insofar as appropriate cases are selected (e.g., those with non-high-risk aberrations), long-term response could bemaintained or relatively long-term therapy could be accomplished even in SD.

142

ポスター発表（Poster Presentation）

P13-3
津島
末永

隆史、小林
孝生

実臨床におけるダラツムマブの安全性と有効性についての検討
The safety and efficacy of daratumumab in a real world data
宏紀、寺尾

俊紀、安部

佳亮、三浦

大典、成田

健太郎、北館明宏、竹内正美、

Takafumi Tsushima, Hiroki Kobayashi, Toshiki Terao, Yoshiaki Abe, Daisuke Miura, Kentaro Narita, Akihiro Kitadate,
Masami Takeuchi, Kosei Matsue

亀田総合病院 血液腫瘍内科

Department of Medicine,Kameda Medical Center, Japan

Daratumumab is new monoclonal antibody which was approved in patients with relapsed or refractory multiple myeloma(RRMM). Phase 3 trials showed that daratumumab-based therapy showed deep response and longer PFS in treatment
of RRMM. In a real-world, however, data on daratumumab-based therapy remain limited, because daratumumab
was approved in Japan in November 2017.We reviewed the medical records of patients with RRMM who received
daratumumab therapy in our hospital. A total of 53 patients were included in this analysis. In our cohort, median age
was 74 years and median lines of prior therapy was 4. The overall response rate was 69.4%, and 36.7% of patientsachieved complete response (CR) or better. The proportion of patients who attained CR or better was significantly higher
among patients with <4 prior therapies than those with ≥4 (56.5% vs 19.2%, P=0.009). A higher rate of CR or better wasobserved in the lenalidomide combination group. However, the difference was not statistically significant. Estimatedprogression free survival at 12 months was 60.6% and 24.5% patients attained minimal residual disease negative status.
Common adverse events were hematological toxicities, including neutropenia and lymphopenia. The occurrence of grade
3 or 4 neutropenia and lymphopenia was 35.8% and 45.3%, respectively. However, the rate of febrile neutropenia waslow (3.8%). Infusion-related reactions occurred in 32.1% of patients, but were grade 1 or 2. In conclusion, this analysis
showed that daratumumab combination therapies would be effective and safe in clinical practice.

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143

ポスター発表（Poster Presentation）

P13-4

Updated Analysis of Daratumumab Plus Rd in East Asian and Japanese Relapsed/
Refractory Multiple Myeloma Patients: POLLUX

竹迫 直樹 1、Meletios A Dimopoulos2、飯田 真介 3、岡本 真一郎 4、品川
Sung-Soo Yoon8、Shang-Yi Huang9、Xiang Qin10、Ming Qi10、鈴木 憲史 11

篤司 5、松本

守生 6、小杉浩史 7、Naoki Takezako1, Meletios A Dimopoulos2, Shinsuke Iida3, Shinichiro Okamoto4, Atsushi Shinagawa5, Morio Matsumoto6,

Hiroshi Kosugi7, Sung-Soo Yoon8, Shang-Yi Huang9, Xiang Qin10, Ming Qi10, Kenshi Suzuki111

独立行政法人国立病院機構 災害医療センター 血液内科、2National and Kapodistrian University of Athens,
Athens, Greece、3名古屋市立大学大学院医学研究科 血液・腫瘍内科学、4慶應義塾大学病院 血液内科、
5
日立総合病院 血液・腫瘍内科、6国立病院機構 渋川医療センター 血液内科、7大垣市民病院 血液内科、
8
Seoul National University Hospital, Seoul, Korea、9National Taiwan University Hospital, Taipei, Taiwan、
10
Janssen Research & Development, LLC, Spring House, PA, USA、11日本赤十字社医療センター 血液内科

Department of Hematology, National Hospital Organization Disaster Medical Center of Japan, Tachikawa, Japan, 2National and

1

Kapodistrian University of Athens, Athens, Greece, 3Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan,

Keio University Hospital, Tokyo, Japan, 5Hitachi General Hospital, Hitachi, Japan, 6Department of Hematology, National Hospital

4

Organization Shibukawa Medical Center, Shibukawa, Japan, 7Department of Hematology, Ogaki Municipal Hospital, Ogaki,

Japan, 8Seoul National University Hospital, Seoul, Korea, 9National Taiwan University Hospital, Taipei, Taiwan, 10Janssen Research& Development, LLC, Spring House, PA, USA, 11Japanese Red Cross Medical Center, Department of Hematology, Tokyo, Japan

The phase 3 POLLUX study showed significant clinical benefit of adding daratumumab (D) to lenalidomide/
dexamethasone (Rd) in RRMM pts after first relapse. Here, we conducted a subgroup analysis of East Asian (EA; Japan,
Korea, Taiwan)/Japanese (J) pts. Pts were randomized 1:1 to D-Rd (52 EA/21 J; 16 mg/kg IV QW Cycles 1-2, Q2W
Cycles 3-6, Q4W until progression) or Rd (44 EA/15 J) only. At a median follow-up of 32.2 mo (EA) and 28.9 mo (J),PFS was longer with D-Rd vs Rd (EA: median not reached [NR] vs 13.8 mo; HR, 0.41; 95% CI, 0.23-0.71; 24-mo PFS
66% vs 29%; J: median NR vs 17.6 mo; HR, 0.28; 95% CI, 0.10-0.77; 24-mo PFS 73% vs 22%). In both EA and J pts,
deeper responses including ≥CR rate (EA: 53% vs 21%; J: 50% vs 7%), and ≥VGPR rate (EA: 77% vs 40%; J: 80%
vs 33%) were higher with D-Rd vs Rd. MRD-negative rates at 10-5 sensitivity threshold were higher with D-Rd vs Rd
in EA (21% vs 5%) and J (24% vs 7%) subgroups. Rates of all-grade pneumonia for D-Rd vs Rd were 24% vs 21% in
EA pts and 10% vs 33% in J pts, respectively. In aggregate, these findings are consistent with results from the overall
study population in terms of improved PFS, ORR, and MRD-negative rates, and absence of new safety signals. Althoughsample sizes were small, these data support the addition of D to Rd in EA/J RRMM pts. Updated EA/J data will bepresented based on >3 y median follow-up, and will include an analysis of elderly (≥75 y) J pts.

144

ポスター発表（Poster Presentation）

P13-5
松本

ELd 療法の長期効果が期待できる患者の解析
Analysis of patients who can expect long-term effects of ELd therapy

守生 1、田原研一 1、三原正大 1、明石直樹 1、磯田淳 1、澤村守夫 2

Morio Matsumoto , kenichi Tahara , Masahiro Mihara , Naoki Akashi , Atsushi Isoda1, Morio Sawamura2
1

1

1

1

1

国立病院機構渋川医療センター 血液内科、2国立病院機構渋川医療センター 臨床研究部

Department of Hematology, National Hospital Organization Shibukawa Medical Center, Japan, 2Department of Clinical1

Research, Japan[Background] Triplet therapy has been used for patients with relapsed/refractory multiple myeloma (RRMM) but it is notclear which regimen to use for which patient. We examined what patients Elotuzumab + lenalidomide + dexamethasone
therapy (ELd therapy) is suitable for.
[Method] The subjects were 24 patients with RRMM who received ELd therapy from December 2016 to December
2018. The age at the beginning of administration is 54 to 88 years old, and the number of prior regimen is 1 to 10. Ig typeis IgG 13 cases, IgA 6, IgD 1, and BJP 4. In IMWG uniform response criteria just before ELd therapy, VGPR was 1 case,PR 4, SD 8, PD 11. There were 22 patients with lenalidomide treatment history, of which lenalidomide resistance was 15
cases.
[Result] After 2 to 28 cycles of ELd therapy, 2 cases were sCR, VGPR 3, PR 4, SD 8, and PD 7. The median progression- free survival (PFS) overall was 144 days. Median PFS for patients with more than 3 regimens was 71 days. Median
PFS for lenalidomide resistant patients was 63 days.
[Discussion] Seven patients were able to administer for more than 1 year, all cases were within 2 prior regimens, 4 ofthem had a response of VGPR or higher. Two patients who had PR obtained by Rd therapy and two patients who received
first administration of lenalidomide at 2nd line with myeloma progressing slowly got deep response greater than VGPR.
However, in patients with lenalidomide resistance and 3 prior regimens or more, ELd therapy was thought to be unlikely
to extend deep response, PFS.

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145

ポスター発表（Poster Presentation）

P13-6

実臨床における再発・難治性骨髄腫患者に対する ERd 療法の効果
Efficacy of elotuzumab plus lenalidomide/dexamethasone in patients with relapsed/refractory multiple myeloma in the real-world practice setting

添田 沙織 1、山下
小松 則夫 6、安井卓也 1、磯田 淳 2、鈴木
寛 7、今井 陽一 7、石橋

一史 3、木口 亨 4、田中真理子 8、田村 秀人 9

紀奈 5、田中

淳司 5、佐々木純 6、Saori Soeda1, Takuya Yamashita1, Atsushi Isoda2, Kazuhito Suzuki3, Toru Kiguchi4, Norina Tanaka5, Junji Tanaka5,
Makoto Sasaki6, Norio Komatsu6, Hiroshi Yasui7, Yoichi Imai7, Mariko Ishibashi8, Hideto Tamura91

聖路加国際病院 血液内科、2国立病院機構渋川医療センター 血液内科、
3
東京慈恵会医科大学附属柏病院 腫瘍・血液内科、4中国中央病院 血液内科、5東京女子医科大学 血液内科、
6
順天堂大学医学部順天堂医院 血液内科、7東京大学医科学研究所 血液腫瘍内科、8日本医科大学微生物学・免疫学、
9
日本医科大学血液内科 血液内科
Hematology Department, Luke's International Hospital, Japan, 2Department of Hematology, National Hospital Organization

1

Shibukawa Medical Center, Japan, 3Division of Clinical Oncology/Hematology, the Jikei University Kashiwa Hospital, Japan,
Department of Hematology, Chugoku Central Hospital, Japan, 5Department of Hematology, Tokyo Women’s Medical

4

University, Japan, 6Division of Hematology, Department of Internal Medicine, Juntendo University School of Medicine, Japan,
Department of Hematology/Oncology, The Institute of Medical Science, The University of Tokyo, Japan, 8Department of

7

Microbiology and Immunology, Nippon Medical School, Japan, 9Department of Hematology, Nippon Medical School, Japan

Introduction: Elotuzumab (ELO) targets SLAMF7 expressed on the surface of multiple myeloma (MM) cells. A phase 3
clinical trial of ELO plus lenalidomide/dexamethasone (ERd) showed a high response rate in patients with t(4;14), which
was correlated with SLAMF7 expression. There are few studies on the efficacy of ERd in clinical practice, and therefore
we evaluated its efficacy in Japanese patients with relapsed/refractory MM (RRMM).
Methods and Results: This was a multicenter, retrospective cohort study. We reviewed 55 patients diagnosed with
RRMM and treated with ELO from 2016 to 2018. The median age was 69 (range 49–87) years. The median number ofprior therapies before ELO treatment was 2 (1–12) and median time to first ERd from diagnosis was 2.9 (0.2–16.2) years.
Thirty (55%) patients were refractory to lenalidomide. The overall response and clinical benefit rates (>stable disease)were 45% and 76%, respectively. The median time to next treatment (TTNT) and overall survival (OS) time were
3.0 (0.1–18.7) and not reached (0 –24.6) months, respectively. Subgroup analysis showed that patients with >2 priortherapies had worse response and poorer survival rates compared with others, and that t(4;14)+ patients did not havebetter responses and outcomes.
Conclusion: TTNT were significantly shorter in our study compared with the phase 3 trials because ours included
heavily treated patients. Further study will reveal the prognostic factors to predict patient populations with goodoutcomes after ERd therapy.

146

ポスター発表（Poster Presentation）

大山

悠、本田

ポスター

P14-1

血清 ICTP が高値を示す形質細胞腫瘍患者におけるボルテゾミブ投与の有効性
Bortezomib overcomes poor prognosis conferred by high serum C-terminal telopeptide oftype I collagen in patients with untreated plasma cell disorder
晃、遠山

和博、黒川

14

峰夫

Yu Oyama, Akira Honda, Kazuhiro Toyama, Mineo Kurokawa

東京大学医学部附属病院 血液・腫瘍内科

Department of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan

Serum C-terminal telopeptide of type I collagen (sICTP) is a well-known biochemical marker of bone remodeling.
Although several reports showed the relationship between a high level of sICTP and poor prognosis in multiple myeloma
patients, little is known about the efficacy of bortezomib in high sICTP patients. In this single center retrospective
study, we assessed the association between sICTP and the prognosis of plasma cell disorder patients. Serum ICTP wasmeasured in 67 patients (30 patients were firstly treated with bortezomib, and 37 were firstly treated without proteasome
inhibitors). High sICTP (above upper normal limit: 4.5 mg/l) tended to be associated with worse 2-year OS (79% versus
95%, P=0.13) and significantly correlated with worse 2-year bone fracture-free survival (FFS) than those with low sICTP(68% versus 95%, P<0.03). Serum ICTP may be a useful marker to predict survival in untreated plasma cell disorderpatients, and these results are consistent with previous reports. Interestingly, in the patients treated with bortezomib, thelevel of sICTP had no effect on 2-year FFS (90% with high sICTP versus 100% with low sICTP, P=0.53) and 2-year OS(95% with high sICTP versus 100% with low sICTP, P=1). These results suggest that bortezomib may overcome poor
prognosis conferred by high sICTP in plasma cell disorder patients. Further studies based on more cases are warranted toelucidate the efficacy of bortezomib in high sICTP patients.

ポスター
13

147

ポスター発表（Poster Presentation）

P14-2
柿本

再発又は難治性の多発性骨髄腫に対するニンラーロ ® カプセル使用成績調査における早期中止例の中間解析
The interim analysis of post-marketing surveillance of ixazomib for relapsed/refractory
multiple myeloma, focusing on early discontinued cases

宜秀 1、星野京2

Yoshihide Kakimoto1, Miyako Hoshino2
12

武田薬品工業株式会社 日本オンコロジー事業部メディカルアフェアーズ部、
武田薬品工業株式会社 ジャパンファーマビジネスユニットメディカルアフェアーズ部

Japan Medical Affairs, Japan Oncology Business Unit, Takeda Pharmaceutical Company Limited, Japan, 2Japan Medical Affairs,

1Japan Pharma Business Unit, Takeda Pharmaceutical Company Limited, Japan

Background and objective
Ixazomib (Ninlaro®) is an oral proteasome inhibitor approved for relapsed/refractory multiple myeloma (RRMM) in
combination with lenalidomide and dexamethasone. Since Japan approval in March 2017, we have been conducting a
post-marketing surveillance investigating the safety data up to 6 cycles of ixazomib for RRMM in clinical practice. In
this interim analysis, we focused on early discontinuations.
Results
114 patients (pts) who were available for fixed data and discontinued treatment before 6 cycles were analyzed. Reasonsfor discontinuation were adverse drug reactions (ADRs) 60 pts, insufficient efficacy 41, others 13. Backgrounds of the pts
were median age 71.5 years old, median number of prior regimen 4.0. 95 pts were refractory to any PI and/or IMiDs, 42
pts were PS ≧ 2 and 47 pts were ISS Ⅲ . ADRs reported in more than 10 pts were thrombocytopenia (62pts), diarrhea (37),nausea (17) and vomiting (15), median time to first onset of each ADR was 14, 15, 9 and 10 days, respectively. Maincause of discontinuation due to ADRs were diarrhea (15pts), thrombocytopenia (12), vomiting (9) and nausea (4).
Discussion
In this surveillance, ixazomib tends to be introduced to elderly and frail patients. The main ADRs causing early
discontinuation were thrombocytopenia and gastrointestinal symptoms. Furthermore, common ADRs often occurred
during the first cycle. When prescribing ixazomib, ADR management in early phase is especially important.

148

ポスター発表（Poster Presentation）

守山

喬史、村上

ポスター

P14-3

当院における再発・難治性多発性骨髄腫に対する Carfilzomib の治療成績
Outcome of treatment of relapsed / refractory multiple myeloma with Carfilzomib
裕之、福見

拓也、石川

立則、吉岡

尚徳、牧田

雅典、角南

14

一貴

Takashi Moriyama, Hiroyuki Murakami, Takuya Fukumi, Tatsunori Ishikawa, Takanori Yoshioka, Masanori Makita,
Kazutaka Sunami

国立病院機構岡山医療センター 血液内科

Department of Hematology,National Hospital Organization Okayama Medical Center, Japan

Background and purpose: Various new drugs have markedly improved the survival of patients with relapsed / refractory
multiple myeloma (RRMM). The efficacy of carfilzomib (CFZ), a second-generation proteasome inhibitor (PI), in
combination with dexamethasone (DEX) (Kd) or with lenalidomide and DEX (KRd) for RRMM has been reported. We
investigated the efficacy and safety of Kd and KRd in 30 patients.
Patients and methods: The subjects were 30 patients who had received Kd or KRd between September 2016 andDecember 2018. The treatment response was evaluated according to the IMWG criteria, and the overall response rate(ORR), progression-free survival (PFS) and overall survival (OS) were analyzed.
Results: Of the 30 patients, 15 and 15 received KRd and Kd, respectively. The median age was 68 years (range, 3885 years), and the median number of prior regimens was 4 (range, 1-10). The median ORR and PFS were 40% and
3.7 months in the patients treated with KRd, and 47% and 5.7 in those treated with Kd, respectively. The median OS
was not reached in either group of patients. The adverse events higher than grade 3 (in patients on KRd/Kd) were
thrombocytopenia in 20 patients (9/11), neutropenia in 12 (7/5), and anemia in 16 (5/11).
Discussion: The outcome of treatment with CFZ was poorer compared to that in clinical trials regarding ORR and PFS,
and the toxicities was higher. One possible factor for this is that the number of prior regimens was high. However, CFZ
was also effective in PI-resistant patients, suggesting that CFZ is an effective agent for the treatment of RRMM.

149

ポスター発表（Poster Presentation）

P14-4
木口

亨、野村

当施設における多発性骨髄腫に対するカルフィルゾミブ併用療法の有効性と安全性の検討
Efficacy and safety of carfilzomib containing regimens for multiple myeloma in our
institution
奈穂、岡本

幸代、黒井

大雅、谷

勝真、遠西

大輔、瀨﨑

伸夫

Toru Kiguchi, Naho Nomura, Sachiyo Okamoto, Taiga Kuroi, Katsuma Tani, Daisuke Ennishi, Nobuo Sezaki

中国中央病院 血液内科

Department of Hematology, Chugoku Central Hospital, Japan

We retrospectively analyzed multiple myeloma patients treated with either carfilzomib/dexamethasone (Kd) or KRd
between December 2016 and November 2018.Total numbers of patients were 21(Kd;n=8,KRd;n=13), and bothgroups showed male predominance(Kd 75%,KRd 69.2%).Median age at 1st carfilzomib of Kd and KRd was 71(6076) vs 66(41-78). Numbers of patients with high risk cytogenetics was equal (Kd n=2,KRd n=2), and all patients withextramedullary disease were treated with KRd. Median numbers of previous regimens, ratio of previous Bortezomib
and previous Lenalidomide of Kd and KRd were 1(1-13) vs 1(0-10) ,50% vs 30.8% , and 50% vs 46.2% respectively.
Median numbers of total cycles of Kd and KRd were 5(2-16) vs 4(1-10). ORR of Kd was superior to that of KRd(Kd;87.5%,KRd 76.9%), although PFS at 12months of Kd was inferior to that of KRd( Kd 57.1% vs KRd 83.3%). Patients
who achieved VGPR or better were treated with 2 or less previous regimens. 21 grade 3/4 adverse events(AEs) wereobserved, and 6 patients were discontinued treatment due to AEs (Kd;n=2,KRd;n=4).Major grade 3/4 AEs were anemia(Kd 25%,KRd 23.1%),thrombocytopenia(Kd 50%,KRd 15.4%),Hypertension (Kd;n=1),pneumonitis(Kd;n=2),amyla
se elevation(Kd;n=1),heart failure (Kd;n= 1,KRd;n= 1),DVT (KRd;n=1),and PN (KRd;n=1).Carfilzomib containing
regimens were effective and well tolerated as previously reported. Our findings might suggest the efficacy of theseregimens for newly diagnosed multiple myeloma.

150ポスター発表（Poster Presentation）
ポスター

P14-5

Phase 2 Trial of Pomalidomide + Low-Dose Dexamethasone + Daratumumab in Relapsed
Refractory Multiple Myeloma: Safety, Efficacy, and Immune Profile

14

David S. Siegel1, Gary J Schiller2, Christy Samaras3, Jesus Berdeja4, Siddhartha Ganguly5, Jeffrey Matous6, Kevin Song7,
Christopher S. Seet8, Giampaolo Talamo9, Mirelis Acosta-Rivera10, Michael Bar11, Donald Quick12, Bertrand Anz13,

Gustavo Fonseca14, Donna Reece15, Amit Agarwal16, Weiyuan Chung16, William Pierceall16, Faiza Zafar16, Nizar J. Bahlis17
1

John Theurer Cancer Center, Hackensack University Medical Center, Hackensack, NJ, United States, 2David Geffen School of

Medicine at University of California, Los Angeles, CA, United States, 3Cleveland Clinic, Cleveland, OH, United States, 4Sarah

Cannon Research Institute, Nashville, TN, United States, 5The University of Kansas Cancer Center, Fairway, KS, United States,

Colorado Blood Cancer Institute, Denver, CO, United States, 7Vancouver General Hospital, Vancouver, BC, Canada, 8University

6of California, Los Angeles Medical Center, Los Angeles, CA, United States, 9Penn State Hershey Cancer Institute, Hershey, PA,

United States, 10Fundación de Investigación, San Juan, Puerto Rico, 11Stamford Hospital, Stamford, CT, 12Joe Arrington Cancer

Research and Treatment Center, Lubbock, TX, United States, 13Tennessee Oncology, Chattanooga, TN, United States, 14Florida

Cancer Specialists, St Petersburg, FL, United States, 15Princess Margaret Cancer Centre, Toronto, ON, Canada, 16Celgene
Corporation, Summit, NJ, United States, 17University of Calgary, Calgary, AB, Canada

BACKGROUND: Lenalidomide (LEN)-refractory patients (pts) have largely been excluded from recent trials
investigating triplet regimens after ≤ 3 prior treatment (Tx) lines. MM-014 (NCT01946477) is examining pomalidomide(POM)-based Tx in relapsed refractory multiple myeloma (RRMM) pts with first- or second-line LEN Tx failure
immediately prior to study entry. Here, we report results from cohort B (POM + low-dose dexamethasone [LoDEX] +daratumumab [DARA]).
METHODS: RRMM pts with 1-2 prior Tx lines, LEN-based Tx as their most recent regimen, and PD during/after theirlast line of Tx received POM + LoDEX + DARA. Primary endpoint was ORR.
RESULTS: As of April 30, 2018, the ITT population comprised 112 pts (median age 66.5 yrs). All had prior LEN (75%
LEN-refractory). ORR (primary) was 78% (≥ VGPR: 34%); median TTR was 1 mo. 9-mo PFS and TTP were 86%
and 88%. ORR was 86% in LEN-relapsed and 75% in LEN-refractory pts. Most common grade 3/4 hematologic andnonhematologic Tx-emergent AEs were neutropenia (62%; febrile 7%) and pneumonia (7%), respectively. Immune
profiling of peripheral blood (n = 98) showed enhanced proliferative activity in CD4, CD8 (including effector memory
cell subsets), and NK cells following Tx.
CONCLUSIONS: With a median follow-up of 5.6 mos for PFS, the 9-mo PFS rate is promising. ORR was higher andgrade 3/4 neutropenia was lower than previously seen with POM + LoDEX + DARA in later Tx lines. Increases in T
cell proliferation and effector differentiation represent an enhanced immune benefit of POM. Data support earlier use ofPOM-based Tx in RRMM after LEN.

151

ポスター発表（Poster Presentation）

P15-1

再発又は難治性多発性骨髄腫に対する段階的増量レナリドミド療法による治療戦略
Therapeutic strategy with dose-escalating lenalidomide for relapsed or refractory multiple
myeloma

北川 順一 1、金田 裕人 1、山口 公大 1、松本 拓郎 1、中村
清水 雅仁 1、原 武志 4、澤田 道夫 3、鶴見 寿 4

博 1、二宮空暢 1、兼村

信宏 1、笠原

千嗣 2、Junichi Kitagawa1, Yuto Kaneda1, Kimihiro Yamaguchi1, Takuro Matsumoto1, Hiroshi Nakamura1, Soranobu Ninomiya1,

Nobuhiro Kanemura1, Senji Kasahara2, Masahito Shimizu1, Takeshi Hara4, Michio Sawada3, Hisashi Tsurumi4
1

岐阜大学医学部 血液内科、2岐阜市民病院 血液内科、3岐阜赤十字病院 血液内科、4松波総合病院 血液内科

Department of Hematology, Gifu University Graduate School of Medicine, Japan, 2Department of Hematology, Gifu Municipal

1

Hospital, Japan, 3Department of Hematology, Gifu Red Cross Hospital, Japan, 4Department of Hematology, Matsunami General
Hospital, Japan

Introduction: Lenalidomide (Len) plays an important role for the treatment of relapsed or refractory multiple myeloma(RRMM) patients (pts). Attenuation of Len dose is often advocated for unfit/frail pts hardly tolerable for intensive
chemotherapy because of serious adverse events, but the optimal dose reduction strategy is not established. Methods:
We prospectively analyzed 16 pts who had received Len on days 1-21 of each 28-day cycle with a starting dose of 10
mg/day, and 20 mg/day dexamethasone (Dex) on days 1, 8, 15 and 22 of each 28-day cycle until disease progression or
discontinuation for any reason. Len was incremented by 5 mg to 25 mg unless grade (G-) 2 non-hematologic toxicity or
G-3 hematologic toxicity is observed. (UMIN000019917)Results: The median age was 68-year-old (55-83). Five weremale, and 11 female. The median number of prior regimens was 2 (1-3). Two pts had previously received autologous
peripheral blood stem cell transplantation. The median number of course was 12 (1-39). The median maximum dose andfinal dose of Len were 15 mg (10-25 mg, 25 mg; 2 pts) and 15 mg (5-25 mg, 25 mg; 1 pt), respectively. Response rate
was 81.3% that included 6 very good partial response. G-3 hematologic toxicity was observed in 3 pts (neutropenia; 2,thrombocytopenia 1), and G-2-3 non-hematologic toxicity was observed in 12 pts (peripheral neuropathy 2, pneumonia
2, and so on). G-4 toxicity was not observed. Conclusion: This result was comparable to the histological outcomes of
RRMM. Dose-escalating Len strategy might be effective and safe for unfit/frail RRMM pts.

152

ポスター発表（Poster Presentation）

P15-2

敬宏 1、藤岡優樹 1,2、池田

翔 1、西川博嘉 2、髙橋

直人 1

ポスター

小林

高齢未治療多発性骨髄腫における Ld 療法前後の免疫プロファイルの変化と無増悪期間との関連の検討
Correlation between immune profile changes and time to progression in patients with
newly diagnosed multiple myeloma treated with Ld therapy

Takahiro Kobayashi1, Yuki Fujioka1,2, Sho Ikeda1, Hiroyoshi Nishikawa2, Naoto Takahashi1
1

秋田大学大学院医学系研究科 血液内科、2国立がん研究センター 免疫TR分野

15

Department of Hematology, Akita University, Japan, 2Division of Cancer immunology, Exploratory Oncology Research and1

Clinical Trial Center, National Cancer Center, Japan

Background:Novel agents have improved the survival of patients with multiple myeloma (MM) along with deep
response. On the other hand, we sometimes experience the long progression free survival by low-dose lenalidomide anddexamethsone (Ld) therapy in some patients without deep response.
In this study, we evaluated the correlation between immune profile changes and time to progression in patients with
newly diagnosed MM (NDMM) treated with Ld therapy.
Material and Method:We have previously conducted a prospective trial of Ld therapy in 40 patients with NDMM.
Among them, 20 patients were enrolled in this analysis excluding the patients who discontinued Ld therapy due totoxicity or treatment intensification. Peripheral blood mononuclear cells (PBMCs) were obtained before and during 1st
cycle of Ld therapy and analyzed by flow cytometry.
Results:Median age was 77 years old (range 66-86). Median time to progression was 33 months (range 2-70). We
divided into two groups with the 33 months as a cut-off point and evaluated the immune change. As a results, the increaseof granzyme B expression in CD8+ T and NK and NKT cells (the difference between after Ld therapy and before Ld
therapy) were significantly higher in a longer TTP subgroup.
Conclusion:Our data suggest that the immune response at 1st cycle of Ld therapy could be the predictive marker of
longer TTP even without the achievement of deep response. It could be the benefit in some patients especially for frail
elderly patients by avoiding the unnecessary treatment intensification. Further investigation is in progress.

153ポスター発表（Poster Presentation）

P15-3
木下
楠本

レナリドミド治療前後における CRBN 関連遺伝子の発現量変化と遺伝子変異の解析
Analysis of expression levels and mutations in CRBN related genes at pre- and postlenalidomide treatment in multiple myeloma

史緒理、李 政樹、立田 卓登、浅野茂、小松 弘和、飯田 真介

有彩、青木

奨、金森

貴之、戸谷

治仁、成田

朋子、伊藤

旭、

Shiori Kinoshita, Masaki Ri, Takuto Tachita, Arisa Asano, Sho Aoki, Takashi Kanamori, Haruhito Totani, Tomoko Narita,
Asahi Ito, Shigeru Kusumoto, Hirokazu Komatsu, Shinsuke Iida

名古屋市立大学病院 血液・腫瘍内科

Department of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Japan

Lenalidomide (Len) binds to cereblon and alters its substrate specificity which results in anti-tumor effects. This study
was conducted to explore if expression levels of CRBN, IKZF1, IKZF3, CUL4A and KPNA2 mRNAs and mutationsof above genes and TP53, except for KPNA2, myeloma cells were associated with its treatment outcome and toinvestigate their alteration at post treatment. Forty-eight bone marrow specimens were collected just prior to Len plus
dexamethasone (Ld). Expression levels of any of above genes were not significantly associated with the best response,
PFS and OS. When tested and using the ratio to CRBN, poor responders to Ld showed a significantly lower IKZF1/CRBN
ratio than good responders. In addition, the patients with lower ratio of IKZF1/CRBN showed a significantly shorter OS
than those with higher. On the other hand, the patients with higher ratio of KPNA2/CRBN showed a significantly shorter
PFS and OS than with lower. Of the 25 paired BM samples collected at both pre- and post-Ld, most samples showed
reduction of the expression levels of CRBN and increase of IKZF1. In 22 paired samples, no mutations of the following
genes, CRBN, IKZF1, and CUL4A, were observed, while, mutation of TP53 and IKZF3 were observed in 2 samples and1 sample at post Ld, respectively. A low ratio of IKZF1/CRBN and high ratio of KPNA2/CRBN may predict for the poor
efficacy to Ld. Reduced CRBN expression was observed in most refractory patients to Ld, suggesting an existence oflower dependence on cereblon and related pathways during development of Len resistance.

154ポスター発表（Poster Presentation）

P15-4
宮崎

寛至、石田

ボルテゾミブとレナリドミドに不応となった多発性骨髄腫症例の予後研究
Survival of Patients with Multiple Myeloma That Is Refractory to Both Bortezomib andLenalidomide: A Retrospective Study
禎夫、鈴木

憲史

ポスター

Kanji Miyazaki, Tadao Ishida, Kenshi Suzuki

日本赤十字社医療センター 血液内科

Department of Hematology, Japanese Red Cross Medical Center, Japan

15

Introduction: Patients with multiple myeloma that is refractory to both bortezomib and lenalidomide show poor survival.
Several new drugs have become available in recent years. The present study aimed to evaluate the survival of suchpatients and assess the effectiveness of the new drugs, autologous transplantation and allogeneic transplantation.
Methods: This retrospective study reviewed the medical records of patients with multiple myeloma who received
treatment between February 2002 and January 2018 at our institution. Patients with myeloma refractory to bothbortezomib and lenalidomide were selected. The primary outcome was overall survival.
Results: The study included 103 patients. New drugs were used in 72 (69.9%) patients, and their OS was significantly
better than that of the remaining 31 (30.1%) patients who did not receive those agents (p < 0.001). Total 15 patients
underwent autologous transplantation without allogeneic transplantation and total 10 patients underwent allogeneictransplantation. Their OS was similar to that of those who did not undergo transplantation. In the 72 patients who weretreated using new drugs carfilzomib, ixazomib, elotuzumab, and daratumumab-based therapies were associated with
better OS. The OS of patients administered only 1 new drug was worse than that of patients administered 2 new drugs (p= 0.005).
Conclusions: New drugs are associated with improved survival in patients with double refractory myeloma. Autologous
and allogeneic transplantation are not associated with improved survival.

155

ポスター発表（Poster Presentation）

P15-5

移植後微小残存病変に対するエロツズマブ併用体外増幅ＮＫ細胞輸注療法第一例目の報告
Ex-vivo expanded NK cell therapy combined with Elotuzumab for MRD after autologous
stem cell transplantation - A report of the first case -萩原 將太郎 1、王 艶華 1、小林 博人 2、加藤 豊 1、飯塚
吉永 健太郎 1、志関 雅幸 1、菅野 仁 2、田中 淳司 1

有希 1、田中紀奈 1、町島

智人 3、石山

みどり 1、

Shotaro Hagiwara1, Yun Hua Wang1, Hirohito Kobayashi2, Yutaka Kato1, Yuki Iizuka1, Norina Tanaka1, Tomohito Machishima3,

Midori Ishiyama1, Kentaro Yoshinaga1, Masayuki Shiseki1, Hitoshi Kanno2, Junji Tanaka1
1

東京女子医科大学医学部 血液内科学講座、2東京女子医科大学医学部 輸血・細胞治療部、3済生会栗橋病院 血液内科

Department of Hematology, Tokyo Women's Medical University, Japan, 2Department of Transfusion Medicine and Cell

1

Processing, Tokyo Women's Medical University, Japan, 3Department of Hematology, Saiseikai Kurihashi Hospital, Japan

Recent advances of monoclonal antibodies provide a potent anti-myeloma effect based on antibody-dependent
cytotoxicity (ADCC). Elotuzumab (Elo) is a monoclonal antibody which binds to SLAMF7 on the surface of myeloma
cells and induces ADCC by NK cells. Therefore, we conduct the clinical trial of ex-vivo expanded NK cell infusion
therapy in combination with Elo-Lenalidomide-Dexamethasone (ELD) for minimal residual disease (MRD) after
autologous stem cell transplantation. We report the first case of the study. A 60-year-old male presented with acute renal
failure. We diagnosed him with IgA lambda multiple myeloma. Cytogenetic analysis revealed IgH-FGFR3 positive.
He was treated with Bortezomib-Dexamethasone regimen followed by autologous stem cell transplantation with
MEL200mg/m2. After the transplantation, he achieved complete remission; however, the multi-color flow cytometry
showed MRD positive (1.1x10-5). Then he proceeded to NK cell therapy, and 100ml of peripheral blood was obtainedfor NK cell expansion. The 1.0 x 107/kg of NK cells were infused on day 2 of ELD regimen without any adverse event.
We repeated another 3 courses of NK cell infusion with ELD. The infused NK cells were 3.8 x 107, 2,27 x107, 2.37x107/
kg, respectively. During the second course of ELD, he developed parotitis which was promptly resolved with antibiotics.
After completion of the treatment, the multi-color flow cytometry showed MRD negative (<0.0 x 10-5). We experienced
the first case of ex-vivo expanded NK cell therapy without severe adverse event. Further study is warranted.

156

ポスター発表（Poster Presentation）

P16-1

直樹 1、三原正大 1、田原研一 1、磯田淳 1、松本守生 1、澤村

守夫 2

ポスター

明石

ポマリドミド＋低用量デキサメタゾン（Pd）療法の有効性と安全性～当院の再発難治性多発性骨髄腫（RRMM）26 例の後方視的解析～
Efficacy and safety of pomalidomide and low dose dexamethasone ; retrospective analysisof 26 relapse and refractory multiple myeloma in our hospital

Naoki Akashi1, Masahiro Mihara1, Kenichi Tahara1, Atsushi Isoda1, Morio Matsumoto1, Morio Sawamura2
1

渋川医療センター 血液内科、2渋川医療センター 臨床研究部

15

Department of Hematology, Shibukawa Medical Center, Japan, 2Department of Clinical Research, Shibukawa Medical Center,

1

Japan

157

ポスター

Background : A lot of clinical trials using new drugs are on going for RRMM patients who have resistance toproteasome inhibitor and/or immunomodulatory drugs.
Methods : In our hospital, 26 patients have received pomalidomide and low dose dexamethasone (Pd therapy) fromMay/2015 to May/2018. We evaluated efficacy and safety.
Result : The median age was 68.5 years (54-94). The median number of prior treatment regimens was 4 (2-5). 21 patients
had lenalidomide resistance. The best response was VGPR in 2, PR in 7, SD in 9, and PD in 6. 23 patients discontinued
Pd therapy, 18 of them due to disease progression. The median duration until PD was 3.5 months (1.0-8.5). Grade3 ormore hematological adverse events were neutropenia in 16 patients, anemia in 12, thrombocytopenia in 11, and Grade3
or more infections occurred in 7 patients. Pd therapy was discontinued because of myelosupression in 2 patients,
somnolence in 1.The median PFS of the next therapy of Pd therapy was 3.0 months (2.5-10.0).
Discussion : The best response of Pd therapy and the median duration until PD in our hospital was not inferior to clinical
trials in the past. Frequency of myelosupression and infection was similar to clinical trials, and we suggest the safety of
Pd therapy. The median PFS of the next therapy of Pd therapy was slightly inferior to clinical trials in the past, because
therapy discontinuation due to adverse events made several cases expected longer PFS unevaluable, we guess.

16

ポスター発表（Poster Presentation）

P16-2

当科での Pomalidomide 16 例の使用経験
Experience with the Use of Pomalidomide in Sixteen Patients at Our Department

若林 睦 1、関口 康宣 1、飯塚 弘子 1、瀧澤 春子 1、杉元 啓二 1、坂尻
大久保 光夫 3、中村 紀子 4、澤田 朝寛 4、小松 則夫 5、野口 雅章 1

さくら 1、冨田

茂樹 2、泉浩 2、

Mutsumi Wakabayashi1, Yasunobu Sekiguchi1, Hiroko Iizuka1, Haruko Takizawa1, Keiji Sugimoto1, Sakura Sakajiri1,

Shigeki Tomita2, Hiroshi Izumi2, Mitsuo Okubo3, Noriko Nakamura4, Tomohiro Sawada4, Norio Komatsu5, Masaaki Noguchi1
1

順天堂大学医学部附属浦安病院 血液内科、2順天堂大学医学部附属浦安病院 病理部、順天堂大学医学部附属浦安病院 輸血学研究室、4順天堂大学医学部附属浦安病院 臨床検査医学科、
5
順天堂大学医学部附属順天堂医院 血液内科
3

Department of Hematology, Juntendo University Urayasu Hospital, Japan, 2Department of Pathology, Juntendo University

1

Urayasu Hospital, Japan, 3Blood Transfusion Research Laboratory, Juntendo University Urayasu Hospital, Japan, 4Department ofLaboratory Medicine, Juntendo University Urayasu Hospital, Japan, 5 Department of Hematology, Juntendo University Juntendo

Hospital, Japan[Objective] To verify problems regarding the efficacy, safety of pomalidomide (Pom).
[Subjects and Methods] Data from 16 pts who had received Pom.
[Results] 10 men and 6 women with a median age of 70 years (range: 48-88). IgG in 8, BJP in 4, IgA in 3, and IgD in 1.
Stage I in 2, II in 9, III in 4, and unknown in 1. High-risk chromosomal were in 6, non-high-risk in 8, and unknown in 2.
The median number of prior regimens was 3.5 (range: 1-6), and the median interval from diagnosis was 4.75 years (range:
0.3-8.9). The median dose of Pom was 2.5 mg (1 qod-4). The median number of cycles of Pom was 5 (range: 1-24).
The best response was sCR in 1 PR in 9, SD in 3, and PD in 3. The outcome was survival in 10 and death in 6. AE werecytopenia in 4, malaise and pneumonia in 2, and appetite impaired, nausea, heart failure, febrile neutropenia, numbness,
chest pain, and rash in 1 each; no in 6.
[Discussion] We compared the two groups according to the response: the good response group (GRG) of 10 with PR or
better responses versus the poor response group(PRG) of 6 with SD or worse responses. High-risk chromosomal rate,
dose level of Pom, and number of prior regimens were lower in GRG. Duration of Pom was longer, and survival rate
was higher in GRG. There was no significant difference in the interval from diagnosis until the initiation of Pom. Pom
dose level were lower in GRG, and the data indicated inter-individual differences in the optimal dosage. The data also
indicated the absence of cross-tolerance between Pom and lenalidomide.

158ポスター発表（Poster Presentation）

P16-3
井手

史朗、大原

当院における形質細胞腫を伴う多発性骨髄腫に対する、ポマリドミド・シクロホスファミド・
デキサメタゾン併用療法の使用成績
Pomalidomide, cyclophosphamide, and dexamethasone as an efficient regimen for
extramedullary multiple myeloma
慎、内田

智之、井上

盛浩、華

見、萩原

政夫

Shiro Ide, Shin Ohara, Tomoyuki Uchida, Morihiro Inoue, Hua Jian, Masao Hagihara

永寿総合病院 血液内科

Department of Hematology, Eiju General Hospital, Japan

159

ポスター

Pomalidomide achieved very convincing responses in relapsed and refractory multiple myeloma (RRMM) patients,
including those who are refractory to both lenalidomide and bortezomib. Nevertheless, the improvement of response
either as a remission rate or a duration is an unmet need in a daily clinical situation. In this point of view, the efficacy andsafety of the completely oral regimen, pomalidomide, cyclophosphamide and dexamethasone (PCD) are attracting anattention.
We have analyzed 36 cases of MM patients, which were treated with pomalidomide and dexamethasone (PD) or PCD
therapy in our institute. Primary end point was partial remission or better (ORR). Responses were obtained in 53.5% (8/15)
patients with PCD, while that of PD therapy was 38.1% (8/21).
Extramedullary disease (EMD) is often detected incidentally on imaging or, less commonly, can present with clinicalsymptoms, which is one of risk factors for prognosis. We examined the effect of PD or PCD therapy on MM patientscomplicated with EMD. Responses were obtained in 57% (4/7) patients treated with PCD, including 3 cases with VGPR,
which showed marked reduction of tumor size soon after the treatment. On the other hand, the effect of PD therapy was
as low as 12.5% (1/8). In conclusion, it was considered that cyclophosphamide could be a promising partner to resolve a
resistance in heavily treated MM cases, especially with EMD.

16

ポスター発表（Poster Presentation）

P16-4
淵田

真一 1、角当院におけるポマリドマイド / デキサメタゾン療法 34 例の後方視的検討
Retrospective analysis of pomalidomide with dexametasone for 34 patients with relapsed/refractory multiple myeloma; A single center experience
陽子 2、民西葉子 1、松井紗央梨 1、初瀬

真弓 1、村頭

智 1、島崎千尋 1

Shin-ichi Fuchida1, Yoko Kado2, Yoko Taminishi-Katsuragawa1, Saori Matsui-Maegawa1, Mayumi Hatsuse1,
Satoshi Murakami1, Chihiro Shimazaki1

1

JCHO 京都鞍馬口医療センター 血液内科、2JCHO 京都鞍馬口医療センター 薬剤科

Department of Hematology, JCHO Kyoto Kuramaguchi Medical Center, Japan, 2Department of Pharmacy, JCHO Kyoto

1

Kuramaguchi Medical Center, Japan

Pomalidomide (POM) is an immunomodulatory drug which improved treatment outcomes of relapsed/refractory
multiple myeloma (RRMM) patients who are dual resistant to bortezomib and lenalidomide. We retrospectively analyzed
the safety and efficacy of POM in combination with dexamethasone (POM/DEX) in RRMM treated after June 2015
in our hospital.Thirty four patients (16 male and 18 female) were included in this study. Median age was 71 years old(46-88). Their M-protein were 17 IgG, 8 IgA, 9 BJP, 20 κ and 14 λ types. Median number of previous therapies before
POM/DEX was 4 (2-15). Median cycles of POM/DEX were 6 (1-32). Six patients received POM/DEX for more than
12 months, and two received for more than 24 months with sCR. Overall response rate was 23.5% and disease control
rate of achieving at least stable disease was 82.4%. 1 year overall survival after POM/DEX was 67.5% and 1 year event
free survival was 15.3%. Causes of discontinuation of POM/DEX were progressive disease in 21 cases and adverse
events in 7 cases. Adverse events included Grade 4 myelodysplastic syndrome in 1 case, Grade 3 fever in 1 case, Grade 2
malaise in 4 cases, Grade 1 pneumonitis in 1 case, and Grade 1 skin rash in 1 case. In conclusion, POM/DEX was mostly
used in patients with advanced stage of RRMM, but it was tolerable and effective in these conditions. New combination
therapies with POM are needed to improve efficacy and reduce toxicities.

160ポスター発表（Poster Presentation）

P16-5
矢野

寛樹、中村

ボルテゾミブおよびレナリドミドレジメン抵抗性多発性骨髄腫に対する PomCyDex 療法
PomCyDex therapy for double-refractory multiple myeloma
智幸、中島

貴裕

Hiroki Yano, Tomoyuki Nakamura, Takahiro Nakashima

JA愛知厚生連海南病院 血液内科

Department of Hematology, Kainan Hospital, Japan

161

ポスター

[Background] The combination therapy of pomalidomide(Pom), dexamethasone(Dex), and oral weekly
cyclophosphamide(Cy): PomCyDex(PCD) is reported to be superior to PomDex in ORR and PFS for lenalidomide
refractory multiple myeloma(MM) (Blood 127, 2016). However, there is limited data of PCD for double-refractory or
Japanese patients.
[Method] We analyzed 12 MM patients retrospectively who treated with PCD in our hospital from Nov 2016 to Nov
2018.
[Result] The median age at diagnosis of MM was 64 (range: 35-81). All patients were refractory to both of the regimens
containing bortezomib and lenalidomide. The median number of prior therapy was 5 (2-8), including 5 patients after
ASCT. The median duration from diagnosis to starting of PCD was 3.3 years (0.6-4.9). The median number of PCD
cycles was 4 (1-15). 10 patients were started with reduced doses of PCD according to the toxicity of prior therapy. 11
patients were evaluable of responses, since 1 patient died of injury within first cycle. The ORR was 54.5% (1 CR, 2
VGPR, and 3 PR), in particular, 2 of 3 patients with adverse cytogenetics achieved more than VGPR. Moreover, 3 of 5
patients with elevation of LDH at the starting of PCD achieved more than PR. 2 patients with prior therapy of PomDex,
however, achieved no responses. 3 patients (1 CR, 1 VGPR, and 1 SD) could continue PCD over than one year. The
median PFS and OS from the starting of PCD was 5.3 and 13.4 months, respectively.
[Conclusion] PCD appears to be useful for double-refractory MM including patients with adverse cytogenetics oraggressive progression.

16

ポスター発表（Poster Presentation）

P17-1

Development of a Predictive Model of Multiple Myeloma Patient Outcomes Based on
Treatment Sequencing Using the Connect® MM Patient Registry

Sundar Jagannath1, Robert M. Rifkin2, Cristina J. Gasparetto3, Kathleen Toomey4, Brian G.M. Durie5, James W. Hardin6,

Howard Terebelo7, Lynne Wagner8, Mohit Narang9, Shankar Srinivasan10, Lihua Yue10, Amani Kitali10, Gail Larkins10,
Amit Agarwal10, Rafat Abonour11

Mount Sinai Hospital, New York, NY, USA, 2US Oncology Research, Rocky Mountain Cancer Centers, Denver, CO, USA, 3Duke

1

University Medical Center, Durham, NC, USA, 4Steeplechase Cancer Center, Somerville, NJ, USA, 5Cedars-Sinai Samuel Oschin

Cancer Center, Los Angeles, CA, USA, 6University of South Carolina, Columbia, SC, USA, 7Providence Cancer Institute, Southfield,
MI, USA, 8Wake Forest School of Medicine, Winston-Salem, NC, USA, 9US Oncology Research, Maryland Oncology Hematology,

Columbia, MD, USA, 10Celgene Corporation, Summit, NJ, USA, 11Indiana University Simon Cancer Center, Indianapolis, IN, USA

Background: Remitting-relapsing nature of multiple myeloma (MM) and availability of several drugs highlight the need
to better understand sequencing and impact on outcomes. Patients with newly-diagnosed MM are commonly treated withproteasome inhibitor (PI), immunomodulatory (IMiD®) agent (lenalidomide or pomalidomide), or both. Recent phase
3 trials exploring novel combinations at relapse may not reflect real-world outcomes, as they are limited by enrollment
criteria. With data from the Connect MM registry, we utilized a novel model to test outcomes based on treatment
sequencing.
Methods: Treatment transitions were analyzed at disease progression as recorded by treating physician and each patient
could have >1 transition (recorded until sixth line). Median and 3-year OS were estimated for each transition from thestart of post-progression therapy (stratified covariate adjusted curves).
Results: A total of 1523 treatment transitions occurred in 856 patients. Fewer treatment transitions occurred with eachsubsequent line of therapy: 856 (lines 1-2); 385 (lines 2-3); 175 (lines 3-4); and lower for subsequent lines. Median OSfrom first relapse was longest for patients who received IMiD agent and then IMiD agent+PI (n=66 transitions; 61.9
months) or received an IMiD agent+PI and then another IMiD agent+PI (n=41 transitions; 61.9 months).
Conclusions: Initiation of treatment with a IMiD agent±PI followed by IMiD agent+PI after progression is beneficial topatients; may provide persistent immune modulation even in patients with progression on IMiD agent-based regimens.
This model may provide useful information on optimal sequencing as more agents enter clinical practice.

162

ポスター発表（Poster Presentation）

P17-2

Connect® MM Registry: Treatment Choices and Outcomes for Patients with Multiple
Myeloma after Relapse on Lenalidomide Maintenance Therapy

Sundar Jagannath1, Mohit Narang2, Sikander Ailawadhi3, Robert M. Rifkin4, Howard R. Terebelo5, Kathleen Toomey6,

Brian G.M. Durie7, James W. Hardin, Cristina J. Gasparetto9, Lynne Wagner10, James Omel11, Shankar Srinivasan12,

Amani Kitali12, Amit Agarwal12, Rafat Abonour13
1

Mount Sinai Hospital, New York, NY, USA, 2US Oncology Research, Columbia, MD, USA, 3Mayo Clinic, Jacksonville, FL, USA,

Rocky Mountain Cancer Centers US Oncology, Denver, CO, USA, 5Providence Cancer Institute, Novi, MI, USA, 6Steeplechase4

Cancer Center, Somerville, NJ, USA, 7Cedars-Sinai Medical Center, Los Angeles, CA, USA, 8University of South Carolina, Columbia,

SC, USA, 9Duke University Medical Center, Durham, NC, USA, 10Wake Forest School of Medicine, Winston-Salem, NC, USA,

Myeloma Research Advocate/Advisor Grand Island, NE, USA, 12Celgene Corporation, Summit, NJ, USA, 13Indiana University,

11

Indianapolis, IN, USA

163

ポスター

Background: Many patients with MM receive lenalidomide maintenance therapy regardless of transplant. However, data
are lacking on the nature of relapse and treatment choices for patients progressing on lenalidomide maintenance therapy.
Methods: Patterns of relapse, second-line treatment choice, and outcomes were analyzed in transplant eligible andineligible patients progressing on ≤ 15 mg lenalidomide maintenance therapy with second-line regimen initiation < 3months after first progression using data from the largely US community-based (84% of sites) Connect MM Registry(N=3011).
Results: As of 1/15/18, 2939 patients were treated; 1109 entered 2L, 234 of which received lenalidomide maintenancetherapy in 1L. Of those, 52% experienced symptoms at time of relapse (n=122) and 47% had nonsymptomatic relapse(n=112). A PFS benefit was observed with triplet+ (≥ 3 agents; n=112) vs doublet (≤ 2 agents; n=122) regimens (15.0 vs
9.0 mo; HR: 0.68) in 2L. PFS and OS benefits were observed with regimens containing IMiD agent® (lenalidomide or
pomalidomide) + PI versus PI alone (without IMiD agents) (PFS: 13.1 vs 10.2 mo; HR, 0.67; OS: 44.3 vs 25.8 mo; HR,0.53) in second-line. Rates of serious adverse events were similar among treatment groups: 43%, 35%, and 33% with
IMiD agent + PI (n=61), IMiD agent (without PI; n=57), and PI (n=102), respectively.
Conclusions: These data describing relapse patterns, second-line treatment choice and survival outcomes after relapse on
lenalidomide maintenance therapy may be used to inform treatment choices in this patient population.

17

ポスター発表（Poster Presentation）㊝ P17-3

Pomalidomide + Bortezomib + Low-Dose Dexamethasone in Relapsed / Refractory
Multiple Myeloma After 1 Prior Line of Therapy: A Subanalysis of OPTIMISMM

Kosei Matsue1, Meletios Dimopoulos2, Katja Weisel3, Philippe Moreau4, Larry D. Anderson Jr5, Darrell White6,

Jesus Miguel San7, Pieter Sonneveld8, Monika Engelhardt9, Matthew Jenner10, Jan Dürig11, Michel Pavic12, Morten Salomo13,
Xin Yu14, Tuong Nguyen Vi14, Tsvetan Biyukov15, Teresa Peluso15, Paul Richardson16

1

Kameda Medical Center, Kamogawa-shi, Chiba, Japan, 2National and Kapodistrian University of Athens, Athens, Greece,

University Hospital of Tuebingen, Tuebingen, Germany, 4University Hospital Hôtel-Dieu, Nantes, France, 5University of Texas

3Southwestern Medical Center, Dallas, TX, United States, 6Dalhousie University and Queen Elizabeth II Health Sciences Centre,

Halifax, Canada, 7Clinica Universidad de Navarra, CIMA, IDISNA, Pamplona, Spain, 8Erasmus MC Cancer Institute, Rotterdam,

the Netherlands, 9Universitätsklinikum Freiburg, Freiburg, Germany, 10Southampton General Hospital, Southampton, United
Kingdom, 11University Hospital Essen, Essen, Germany, 12Centre Hospitalier Universitaire De Sherbrooke (CHUS) - Centre deRecherche Clinique Etienne-Le Bel (CRCELB) Hopital Fleurimont, Sherbrooke, Canada, 13Copenhagen University Hospital,

Rigshospitalet, Kobenhavn, Denmark, 14Celgene Corporation, Summit, NJ, United States, 15Celgene International, Boudry,

Switzerland, 16Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute,
Harvard Medical School, Boston, MA, United States

BACKGROUND: In the phase 3 OPTIMISMM trial (NCT01734928) of relapsed / refractory multiple myeloma (RRMM)
patients (pts) who had 1-3 prior regimens and were 100% lenalidomide (LEN) pretreated, pomalidomide, bortezomib,
and low-dose dexamethasone (PVd) significantly improved PFS vs Vd in the ITT population (median PFS 11.2 vs 7.1
mos; HR 0.61; P < .0001), with manageable safety and no negative impact on health-related QoL in evaluable pts despite
longer Tx with PVd. Here, we report safety and efficacy in LEN-refractory (LEN-ref) and LEN-nonrefractory (LENnonref) pts after 1 prior line of therapy (LOT).
METHODS: Pts treated with ≥ 2 cycles of prior LEN were randomized 1:1 to receive PVd or Vd (21-day cycles).
Primary endpoint was PFS.
RESULTS: As of October 26, 2017, 129 pts with 1 prior LOT were LEN-ref (64 PVd; 65 Vd) and 97 were LEN-nonref(47 PVd; 50 Vd). Most baseline characteristics were similar across groups. With a median follow-up of 16.4 mos, median
PFS with PVd vs Vd after 1 prior LOT was 17.8 vs 9.5 mos in LEN-ref and 22.0 vs 12.0 mos in LEN-nonref pts. ORR
was 86% vs 51% in LEN-ref and 96% vs 60% in LEN-nonref pts. Neutropenia, thrombocytopenia, and infection werethe most common grade 3/4 toxicities.
CONCLUSIONS: To date, OPTIMISMM is the only phase 3 trial addressing treatment of LEN-pretreated RRMM pts
in early lines and the first to report data in LEN-ref pts after first relapse. These results reaffirm the safety and efficacy
of PVd in pts for whom LEN is no longer a treatment option, including LEN-ref pts, supporting its use as second-line
therapy in RRMM.

164

ポスター発表（Poster Presentation）

P17-4

RRMM に対するポマリドミド＋ボルテゾミブ＋低用量デキサメタゾン（PVd）併用療法 :OPTIMISMM 試験 日本人サブグループ解析
Pomalidomide + Bortezomib + Low-Dose Dexamethasone (PVd) in Relapsed / Refractory
Multiple Myeloma: OPTIMISMM Japanese Subgroup Analysis

角南 一貴 1、末永 孝生 2、鈴木 憲史 3、竹迫 直樹 4、品川
Tsvetan Biyukov7、Teresa Peluso7、Paul Richardson8

篤司 5、櫻井早苗 6、玉越裕巳 6、Kazutaka Sunami1, Kosei Matsue2, Kenshi Suzuki3, Naoki Takezako4, Atsushi Shinagawa5, Sanae Sakurai6, Hiromi Tamakoshi6,

Tsvetan Biyukov7, Teresa Peluso7, Paul Richardson81

独立行政法人国立病院機構 岡山医療センター 血液内科、2医療法人鉄蕉会 亀田総合病院 血液・腫瘍内科 、3
日本赤十字社医療センター 骨髄腫アミロイドーシスセンター、4独立行政法人国立病院機構 災害医療センター 血液内科 、5株式会社日立製作所 日立総合病院 血液腫瘍内科、6セルジーン株式会社、7Celgene International Sàrl、
8
Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer InstituteNational Hospital Organization Okayama Medical Center, Okayama, Japan, 2Kameda Medical Center, Chiba, Japan, 3Japanese

1

Red Cross Medical Center, Tokyo, Japan, 4National Hospital Organization Disaster Medical Center, Tokyo, Japan, 5Hitachi General
ポスター

Hospital, Ibaraki, Japan, 6Celgene K.K., Tokyo, Japan, 7Celgene International Sàrl, Boudry, Switzerland, 8Dana-Farber Cancer

Institute, Boston, MA, USA

17

BACKGROUND: In the phase 3 OPTIMISMM trial (NCT01734928), PVd showed significantly improved PFS (median
11.2 vs 7.1 mos, HR, 0.61, P < .0001) and a manageable safety profile vs Vd in RRMM patients (pts) who had 1-3 priorregimens and were 100% lenalidomide (LEN) pretreated. Here, we present efficacy and safety in Japanese pts.
METHODS: Pts randomized 1:1 to PVd or Vd received 21-day cycles (C) of pomalidomide 4 mg/day, days 1-14 (PVdarm only), bortezomib (BORT) 1.3 mg/m2, days 1, 4, 8, and 11 C1-8 and on days 1 and 8 C9+, and dexamethasone 20
mg/day (10 mg/day if > 75 yrs), days of and after BORT.
RESULTS: Of 17 pts enrolled in Japan (12 PVd; 5 Vd), 13 were LEN refractory (8 PVd; 5 Vd). Median age was 72 vs
73 yrs in PVd vs Vd arms and 58% vs 80% were male. Pts in both arms had a median of 1 prior line of therapy (range1-2); 67% vs 60% had prior BORT. Treatment (Tx) is ongoing in 7 vs 1 pt; 4 vs 3 pts discontinued due to progressive
disease. Median Tx duration was 14.5 vs 4.0 mos. Median PFS with PVd vs Vd was 17.6 vs 4.4 mos and ORR was 100%
vs 60%; median follow-up 14.8 mos. Median time to response was 0.8 vs 1.5 mos, median duration of response was 16.8
vs 7.4 mos. Grade 3 or 4 treatment-emergent adverse events included infections (5 PVd vs 2 Vd pts), neutropenia (6 PVdpts), thrombocytopenia (2 PVd vs 1 Vd pt), and anemia (1 Vd pt).
CONCLUSIONS: Efficacy outcomes with PVd in a highly LEN-refractory (76%) Japanese subgroup are consistent withthose reported in the overall study population. Of note, PVd led to a 100% ORR, with no new safety signals.

165ポスター発表（Poster Presentation）

P17-5

Bortezomib/melphalan/prednisone (VMP) ± Daratumumab in Transplant-ineligible
Newly Diagnosed Multiple Myeloma: ALCYONE Update with Japanese Subanalysis

藤崎 智明 1、石川 隆之 2、高松
Ming Qi6、長藤 宏司 7

博幸 3、鈴木憲史 4、Jianping Wang5、Anupa Kudva5、Susan Wroblewski6、Tomoaki Fujisaki1, Takayuki Ishikawa2, Hiroyuki Takamatsu3, Kenshi Suzuki4, Jianping Wang5, Anupa Kudva5,

Susan Wroblewski6, Ming Qi6, Koji Nagafuji71

日本赤十字社 松山赤十字病院 内科、2神戸市立医療センター 中央病院 免疫・血液内科、金沢大学 血液・呼吸器内科、4日本赤十字社医療センター 血液内科、5Janssen Research & Development, LLC、
6
Janssen Research and Development, LLC、7久留米大学医学部 血液・腫瘍内科部門
3

Department of Internal Medicine, Matsuyama Red-Cross Hospital, Japan, 2Department of Internal Medicine, Division of1

Immuno-Hematology, Kobe General Central Hospital, Japan, 3Department of Hematology/Respiratory Medicine, Kanazawa

University, Japan, 4Department of Hematology, Japanese Red Cross Medical Centre, Japan, 5Janssen Research & Development,

LLC, 6Janssen Research and Development, LLC, 7Division of Hematology and Oncology, Department of Medicine, Kurume
University School of Medicine, Japan

In the primary analysis of the phase 3 ALCYONE study, D-VMP reduced the risk of disease progression or death by
50% in transplant-ineligible newly diagnosed MM. Here, we report updated efficacy and safety data from ALCYONE
and include a subanalysis of Japanese (J) pts. Pts in ALCYONE were randomized 1:1 to VMP (V, 1.3 mg/m2 SC twice
weekly Cycle 1, QW Cycles 2-9; M, 9 mg/m2 PO Days 1-4 Cycles 1-9; P, 60 mg/m2 PO Days 1-4 Cycles 1-9) ± DARA
(16 mg/kg IV QW Cycle 1, Q3W Cycles 2-9, Q4W Cycles 10+ until progression). The median (range) age was 71 (40-93)
y of age, with 30% being ≥75 years of age. Of 616/706 evaluable pts, 16% had high cytogentic risk (del[17p]; t[4;14];t[14;16]). At a median follow-up of 27.8 months, all pts had either discontinued or completed 9 cycles of VMP, with 194(56%) pts in the D-VMP arm continuing to receive DARA monotherapy in Cycles 10+. For D-VMP vs VMP, median
PFS was not reached vs 19.1 mo (HR, 0.43, 95% CI, 0.35-0.54; P<0.0001). Higher response rates (ORR: 91% vs 74%;
³CR: 45% vs 25%; ³VGPR: 73% vs 50%) and MRD-negativity rate (10-5 threshold; 27% vs 7%) were observed with
D-VMP vs VMP, respectively (all P<0.0001). J pts similarly demonstrated prolonged PFS (median NR vs 20.4 mo; HR,
0.31, 95% CI, 0.12-0.79), a higher ≥CR (54% vs 23%), and a higher MRD-negativity rate (42% vs 8%) with D-VMP (n= 24) vs VMP (n = 26). Among the study population, DARA monotherapy was well tolerated with low rates of treatmentemergent adverse events. These findings suggest clinical benefit of D-VMP in the overall study population and J pts of
ALCYONE.

166

ポスター発表（Poster Presentation）

P18-1
小倉
阿部

効果と医療経済の観点からみた造血幹細胞動員促進薬 Plerixafor
Plerixafor is clinically and economically effective as mobilization protocol for peripheral
blood stem cell apheresis

瑞生、愛葉 美奈、塚田 信弘、梨本 淳一郎、余語
有、岡塚 貴世志、石田 禎夫、鈴木 憲史

孝夫、宇藤

唯、佐藤

広太、宮崎

寛至、吉識

由実子、

Mizuki Ogura, Mina Aiba, Nobuhiro Tsukada, Junichiro Nashimoto, Takao Yogo, Yui Uto, Kota Sato, Kanji Miyazaki,
Yumiko Yoshiki, Yu Abe, Kiyoshi Okazuka, Tadao Ishida, Kenshi Suzuki

日本赤十字社医療センター 血液内科

Department of Hematology, Japanese Red Cross Medical Center, Japan

17

ポスター

167

ポスター

BACKGROUND:Autologous hematopoietic stem cell transplantation is effective therapy for the eligible patientsdiagnosed multiple myeloma. Plerixafor is recently used in combination with granulocyte-colony-stimulating factor(GCSF) for peripheral blood stem cell apheresis. Although plerixafor is so expensive drug, its cost-benefit performance is
not well-studied. Thus, we analyzed its efficacy and cost-effectiveness in our hospital. STUDY DESIGN:A retrospective
observational analysis was performed on patients who received stem cell apheresis between Dec. 2013 and Nov. 2018.
Patients were classified in three groups by pre-mobilize regimen, such as G-CSF, cyclophosphamide plus G-CSF, andplerixafor plus G-CSF. We evaluated the apheresis efficiency by collected CD34+ cells, and we assessed cost from thefollowing three point of view, such as cost of drugs, cost of apheresis, and cost of hospital stay. RESULTS:The subjects
analyzed totaled 30 patients. More stem cell were collected in patients who received plerixafor plus G-CSF than patients
received other regimen (median CD34+ harvest was 4.30 vs 2.85 vs 6.50, P = 0.0479(×10^6 per kg of body weight) .
Cost of drugs was higher in patients who received plerixafor plus G-CSF, but cost of apheresis and cost of hospital staywere higher in patients who received Non-plerixafor regimen. CONCLUSIONS:Non-plerixafor regimen led to longer
apheresis and hospitalization, resulted in delays of treatment schedule and increased cost. Plerixafor is clinically andeconomically effective as mobilization protocol for stem cell apheresis.

18

ポスター発表（Poster Presentation）

P18-2

The Safety profile of daratumumab in Japanese patients with relapsed/refractory multiple
myeloma: post-marketing surveillance of the first 12 weeks

宮田 泰彦 1、滝澤遠城 健太郎 1

愛美 1、高岸正幸 2、川合治功 2、藤野明子 3、矢島勉 4、有田恵梨子 4、

Yasuhiko Miyata1, Manami Takizawa1, Masayuki Takagishi2, Haruyoshi Kawai2, Akiko Fujino3, Tsutomu Yajima4, Eriko Arita4,
Kentaro Enjo1

1

Medical Affairs Division, Janssen Pharma K. K.、2Safety Risk Management Division, Janssen Pharma K. K.、
Japan Safety & Surveillance Division, Janssen Pharma K. K.、4Quantitative Sciences Division, Janssen Pharma K. K.

3

Objectives: The post-marketing surveillance (PMS) study is being conducted to determine mainly the safety profile
of daratumumab in Japanese patients with relapsed/refractory multiple myeloma (rrMM) in an actual clinical setting.
Methods: In this PMS study, all the patients with rrMM treated with daratumumab are registered and monitored for all
adverse events (AEs) noted for 52 weeks since November 2017 and the data for the first 12 weeks were presented here.
Results: By the cut-off date (15 November 2018), data were fixed from 155 patients, 5 of whom were excluded due todouble registration or off-label usage. The median age was 69 years (range, 47 to 84); 51% and 30% of patients were 65-74 and ≥75, respectively. The median time since diagnosis was 3.2 years (range, 0.1 to 27.4), and the median number ofprevious therapy was 4.3 (range, 1 to 12) and 50% of the patients received 4 or more previous lines. DRd and DVd wereused in 64.7% and 35.3%, respectively. In total, 253 AEs were reported from 96 patients (64%) and 99 serious eventsfrom 58 patients (38.7%). Infusion reaction occurred among 45 patients (30%) and 11 cases were grade 3/4 but none ofthem led to treatment discontinuation. Serious infection was observed in 8.7% and one patient died of infection. Therapy
was discontinued in 42 patients (28%) overall, including 25 patients due to insufficient response and 10 patients due to
AEs.
Conclusion: This PMS study showed that daratumumab in combination with either Rd or Vd was well tolerated inJapanese patients with rrMM during the initial therapy period.

168ポスター発表（Poster Presentation）

P18-3
板垣
勝谷

ダラツムマブ (Dara) 療法で infusion reaction を起こさない当院の取り組みの検討
A study on the approach of Daratumumab (Dara) treatment without infusion reaction at our
institution

充弘、麻奥 英毅、片山 雄太、寺崎慎也、牟田 毅、岩戸 康治

達哉、幸地

祐、陳之内

文昭、岡谷

健史、今中

亮太、許

鴻平、

Mitsuhiro Itagaki, Hideki Asaoku, Yuta Katayama, Tatsuya Terasaki, Yu Kohchi, Fumiaki Jinnouchi, Takeshi Okatani,
Ryota Imanaka, Kohei Kyo, Shinya Katsutani, Tsuyoshi Muta, Koji Iwato

広島赤十字・原爆病院 血液内科

Department of Hematology, Hiroshima Red Cross Hospital, Hiroshima, Japan

Introduction
Daratumumab (Dara) is an antibody drug and effective against recurrent/refractory multiple myeloma. However, it also
might cause infusion reaction as a severe adverse effect with approximately 50% chance of occurrence. The initial dosage
is set as maximum 100ml/h for reducing the occurrences of infusion reaction at our institution, and before administrationof Dara, we provide inhalation of bronchodilator to patients with medical history of pulmonary disease such as asthma.
We retrospectively examined the occurrences of infusion reaction for 39 patients with Dara treatment at our institution.

Discussion
In the international cooperative clinical trial, it is reported that infusion reaction during Dara treatment occurred
approximately 50%, but the percentage at our institution was approximately 28%. Thus, it is considered that theadjustment of initial dosage would possibly be effective against infusion reaction.

169

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ResultThere were 34 patients for DLd (Daratumumab+Lenalidomide+Dexamethasone) treatment and 5 patients for DVd (Daratumumab+Bortezomib+Dexamethasone) treatment. 11 patients had medical history of allergic disease such as asthma
and drug eruption. 11 patients (28.2%) had infusion reaction with Grade 1-2. Yet, there was no patient discontinued Dara
treatment due to the adverse events.

18

ポスター発表（Poster Presentation）

P18-4
新行内

IRd 療法の服薬アドヒアランス向上のための薬剤師の役割
Role of pharmacists to improve medication adherence of IRd therapy

健一 1、栗原りか 1、工藤彰 1、蟻川勝 1、飯合等 1、松本

守生 2

Kenichi Shingyouuchi , Rika Kuribara , Akira Kudou , Masaru Arikawa , Hitosi Iiai1, Morio Matsumoto2
1

1

1

1

1

渋川医療センター 薬剤部、2渋川医療センター 血液内科

National Hospital Organization Department of Phamacy Shibukawa Center, Japan, 2National Hospital Organization Department

1of Hematology Shibukawa Medical Center, Japan[Background]
In order to improve the therapeutic effect and to safely continue the treatment for a long period of time, it is important toraise adherence adequacy and to manage adverse events early.
In order to improve medication adherence of IRd therapy for patients with myeloma, the role of our pharmacist was
examined.
[Method] IRd therapy was performed in 8 patients with myeloma between 2017.7 and 2019.1
Initial IRd therapy was initiated in hospital, and the pharmacist provided guidance on medication management such as
explanation and confirmation of administration schedule, medication method, side effects.
For outpatients, a pharmaceutical outpatient clinic was set up in which cancer outpatients can receive active medical carefrom oncology pharmacy specialists, and the pharmacist carried out medication management guidance before a doctor
consulted.
Treatment schedule and side effects including examination value were confirmed using template created on electronic
chart.
[Result]
The pharmacist proposed to the doctor a prescription to seven patients with adverse events, a method of taking aprescription into two patients or a method of taking jelly.
[Discussion] By conducting team medicine including pharmacists and conducting medication management guidance,
adherence of IRd therapy for individual patients is confirmed and expected to be improved.
It is expected that the pharmacist finds an adverse event of the patient at an early stage and suggests an appropriateprescription or a dosing method to the doctor and that the IRd therapy can be continued for a long time.

170ポスター発表（Poster Presentation）

P19-1
稲垣

淳 1、楠本

未治療多発性骨髄腫患者における updated チャールソン併存疾患指数の意義
Impact of updated Charlson comorbidity index on survival in patients with newly diagnosed
multiple myeloma
茂 2、丸茂義晃 1、森芙美子 1、飯田真介 2

Atsushi Inagaki1, Shigeru Kusumoto2, Yoshiaki Marumo1, Fumiko Mori1, Shinsuke Iida2
1

名古屋市立西部医療センター 血液･腫瘍内科、2名古屋市立大学大学院医学研究科 血液･腫瘍内科学

Department of Hematology and Oncology, Nagoya City West Medical Center Japan, 2Department of Hematology and1

Oncology, Nagoya City University Graduate School of Medical Sciences, Japan

18

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171

ポスター

【Introduction】
There is limited evidence regarding the impact of updated Charlson comorbidity index (CCI) on survival in patients with
newly diagnosed multiple myeloma (NDMM).
【Methods】
We retrospectively reviewed 56 patients with NDMM who were admitted to Nagoya City West Medical Center between
May 2011 and January 2019. We evaluated the association between their survival and the 5 following baseline indexes:
CCI, age-adjusted CCI, updated CCI, Barthel index and mini-nutritional assessment (MNA-SF).
【Result】
Baseline characteristics of the 56 patients with NDMM were as follows: median age was 73 years; 82% was ≥65 years;
54% had ECOG-PS ≥2; ISS of I, II, III was 14%, 30%, and 55%, respectively; 14% received autologous stem celltransplantation.
According to the updated CCI, the patients with high score (≥3) had worse prognosis compared to those with low score(50% overall survival [OS], 16.7 vs. 43.3 months; p=0.0356), but neither CCI nor age-adjusted CCI were associated withthe survival. The patients with high BNP levels (BNP≥100 pg/mL) had also worse prognosis compared to those with lowlevels (50%OS, 22.4 vs. 50.7 months; p=0.0345). Updated CCI high score was correlated with malnutrition or high BNPlevels.
【Conclusion】
Updated CCI might be useful to predict prognosis in patients with NDMM. Well-designed prospective studies are
warranted.

19

ポスター発表（Poster Presentation）

P19-2
大原

慎、井手

IMiDs による皮疹に対するステロイド併用下での漸増再投与法の試み
Desensitization to IMiDs-induced skin rush in a patient with multiple myeloma
史朗、内田

智之、井上

盛浩、華

見、萩原

政夫

Shin Ohara, Shiro Ide, Tomoyuki Uchida, Morihiro Inoue, Jian Hua, Masao Hagihara

永寿総合病院 血液内科

Department of Hematology, Eiju general hospital, Japan

Immunomodulatory drugs (IMiDs) for multiple myeloma (MM), such as lenalidomide and pomalidomide, often causerash as an adverse event. When it accelerates to grade2 or higher grades even with an administration of prednisolone(PSL), a discontinuation of treatment is inevitable. Thus, we applied a desensitization protocol under PSL administration(5-20mg/day). Eight patients previously suffered from skin-rash (7 had grade2 or higher grade with lenalidomide, and 1
had grade3 with pomalidomide) were re-started and gradually increased with minimum dose of IMiD as follows; 2.5 or
5mg of initial dose for lenalidomide or 1mg for pomalidomide once a week, followed by twice a week, 3 times a week,
and daily. No reappearance of skin-eruption was observed in all cases, which could receive a continuous treatment.
Nowadays, IMiDs, especially a lenalidomide, is one of key drugs in the treatment of MM. Therefore, those means of
avoiding an adverse should make an important role to improve the results of myeloma treatment.

172ポスター発表（Poster Presentation）

P19-3
奥田

Infusion reaction 軽減のためのダラツムマブ初回低速投与
Slow administration of daratumumab for frail myeloma patients慎也 1、木内

貴章 2、上杉章紀 2、百瀬純子 2、竹林

ちあき 1

Shinya Okuda , Takaaki Kiuchi , Akinori Uesugi , Jyunko Momose , Chiaki Takebayashi1
1

1

2

2

2

JR東京総合病院 血液・腫瘍内科、2JR東京総合病院 薬剤部

Department of hematology and oncology, JR Tokyo general hospital, Japan, 2Department of pharmacy, JR Tokyo general1

hospital, Japan

Infusion-related reactions to daratumumab are common, predominantly occur during the first infusion, and are mostly
mild. However, those reactions are relatively serious for frail patients. We describe five frail patients with multiple
myeloma received daratumumab combination therapy. Frail patients in our hospital received daratumumab 16 mg/kg
at 50 ml/hour for first one hour, at 80 ml/hr thereafter. We gave daratumumab to two myeloma patients (71 and 78 years
men) without infusion-related reaction. An 82-year- old man with Chronic Obstructive Pulmonary Disease had grade 2
infusion-related reaction included bronchospasm after starting 80 ml/hour administration. In subsequent two patients (80years man and 77 years woman), daratumumab 8 mg/kg was diluted with normal saline to a total volume of 500 mL at 9
am and 4 pm, and was infused at 50 ml/hour until completion. Only one patient experienced an infusion-related reaction(grade 1 without interruption). Dexamethasone, d-chlorpheniramine, acetaminophen, and montelukast were given prior
to the first daratumumab infusion. Slow administration of daratumumab may be safe for frail myeloma patients.

ポスター
19

173

ポスター発表（Poster Presentation）

P19-4
鈴木

患者に対してセンシティブな内容（性交渉や避妊等）を説明する医療従事者向け教育プログ
ラムの策定に関する研究
Development of educational program for the medical practitioners who engage in theinterview to the patients about sensitive contents

憲史 1、有田悦子 2、林昌洋 3、服部

豊 4、西村倫子 5、村上博和 6

Kenshi Suzuki1, Etuko Arita2, Masahiro Hayashi3, Yutaka Hattori4, Noriko Nishimura5, Hirokazu Murakami61
3

日本赤十字社医療センター 骨髄腫・アミロイドーシスセンター、2北里大学薬学部医療心理学部門、
虎の門病院薬剤部、4慶應義塾大学薬学研究科、5がん研究会有明病院血液腫瘍科、6群馬大学大学院保健学研究科

Myeloma Amyloidosis Unit, Jepanese Red Cross Medical Center, Japan, 2Department of Medical Psychology, Pharmaceutical

1

Education Research Center, Kitasato University School of Pharmacy, Japan, 3Department of Pharmacy, Toranomon Hospital,
Japan, 4Faculty of Pharmacy, Keio University, Japan, 5Department of Hematology and Oncology, Cancer Institute Hospital,

Japanese Foundation for Cancer Research, Japan, 6Graduate School of Health Sciences, Gunma University, JapanDue to their potential adverse effects to fetuses, it is necessary to talk about sexual intercourse with patients and advise
them on effective methods of contraception, keeping in mind the regulations for medication safety. However, the reality
is that many healthcare professionals are not used to discussing these topics. Therefore, they have some difficulties
during counseling sessions. This situation can create a psychological burden on the patients. To respect the dignity ofpatients, healthcare providers are required to have an exceedingly high level of communication skills.
In this research, we develop training programs to improve patient counseling skills, so that the patients and their families
can feel comfortable and respected during these counseling sessions. After preparing the draft of the training tool,
we conduct a small-scale training. Based on the training results, we revise the training tool draft and a conduct largescale training. Establishment of a final educational program and e-learning systems for the new users. To do so, we first
identify the issues regarding patient counseling of thalidomide and other derivatives. Then, based on the findings, wecreate training programs to enhance communication skills. Once we obtain successful results, we will then introduce thetraining programs to all healthcare providers.
This study has been conducted with the help of research funding from the Ministry of Health, Labor and Welfare in
Japan.

174

ポスター発表（Poster Presentation）

P19-5
中村
別所

裕一、坂本
正美

治療後に高アミラーゼ血症を呈した多発性骨髄腫症例の検討
Hyperamylasemia developing after treatment for multiple myeloma
朋之、奥田糸子、阿久澤

有、伊藤

善啓、脇本

直樹、掛川

絵美、内田

優美子、森

茂久、

Yuichi Nakamura, Tomoyuki Sakamoto, Itoko Okuda, Yuu Akuzawa, Yoshihiro Ito, Naoki Wakimoto, Emi Kakegawa,Yumiko Uchida, Shigehisa Mori, Masami Bessho

埼玉医科大学病院 血液内科

Department of Hematology, Saitama Medical University Hospital, Japan

Hyperamylasemia is a rare adverse event of treatments for multiple myeloma (MM). We report five MM cases presented
hyperamylasemia after drug therapy. Case 1 was a 66-year-old woman treated carfilzomib plus dexamethasone as thethird line chemotherapy for MM. After administration of these drugs, serum amylase activity was elevated up to 546
IU/mL with predominance of pancreatic type and with prominent elevation of serum lipase activity (up to 1002 IU/mL). The elevation of these pancreatic enzymes were reversible, reproducible and related to dosage of carfilzomib. No
signs or symptoms indicating pancreatitis were observed and she received the therapy continuously. Asymptomatic
hyperamylasemia/hyperlipasemia in this case was supposed to be due to direct action of carfilzomib to the pancreas,
although the mechanism was unknown. Case 2 was 77-year-old woman with recurrent MM and presented reversible
hyperamylasemia (up to 325 IU/mL) without elevation of pancreatic type after carfilzomib plus dexamethasone anddaratumumab, lenalidomide plus dexamethasone therapy. Thus, it was indicated that elevation of salivary-type amylase
was caused by destruction of tumor cells after therapy. The other three cases showed mild (grade 2) hyperamylasemia
without elevation of pancreatic type after bortezomib, elotuzumab, or daratumumab therapy in which the exact causes
were undetermined. Although it may be a rare instance, physicians should be aware of hyperamylasemia developing after
treatment for MM and distinguish between drug-induced and disease-related ones by isozyme analysis.
ポスター
19

175

共催セミナー（Co-sponsored Seminars）

ランチョンセミナー（Luncheon seminar）

LS1

Real-World Evidence and Clinical Implications

Sundar Jagannath
Mount Sinai Hospital, New York, NY, USA

While clinical trials remain critical for drug development, their design and strict criteria do not allow resulting datato truly reflect the impact of treatments on the real-world patient population. Thus, real-world evidence (RWE) basedon data from patient experiences are increasingly being used to inform drug development, treatment decisions, andoptimize treatment outcomes. RWE are available from various sources including electronic health records, claims, andpatient registries. In the past, RWE was primarily used by payors but the increasing complexity of healthcare delivery
and clinical trial cost have led to its use by regulators, pharmaceutical companies and physicians to inform treatment
decisions. Disease registries are observational studies that enroll and longitudinally follow a large heterogenous patientgroup with a specific disease or condition. They can discern clinical practice patterns, patient outcomes, and comparative
effectiveness. Long-term follow-up can describe the natural history of disease (e.g., diagnostic and treatment patterns,
clinical and patient-reported outcomes) and indicate if a newly approved drug has been incorporated into recent treatment
pathways, or if side effects differ from those observed in clinical trials. This talk will describe key insights, challenges,
and the value of RWE to clinical practice using an example of the Connect MM Registry, a US, multicenter, prospective
observational cohort study designed to examine diagnostic and treatment patterns, clinical outcomes and quality of life inpatients with multiple myeloma.

178ランチョンセミナー（Luncheon seminar）

LS2
太田

新薬時代における progression-free plateau
Progression-free plateau in era of new agents健介

Kensuke Ohta

LIGARE 血液内科太田クリニック・心斎橋
Hematology Ohta Clinic, Shinsaibashi, JapanThe use of new agents, including proteasome inhibitors, immunomodulatory drugs and/or monoclonal antibodies havesignificantly improved the survival of the patients with multiple myeloma (MM). However, because of appearance ofmany new agents in a short period of time, guidelines to effectively use these agents for the different types and stages of
MM has not sufficiently been organized. To complement a lack of strong evidence, basic theories for effective practice
medicine are needed.
In this, one important point may be how to manage the "progression-free plateau" , which is frequently observed
following various lines of therapy. Recent meta-analysis has suggested that continuous treatment with new agents,
instead of taking treatment-free interval, extend a period of plateau phase, resulting in extension of both PFS and
OS. Secondly, recent observations strongly indicate that insufficient response to the therapies is associated with poor
prognosis, suggesting the importance of achieving plateau with small clone size. Finally, with a Kansai Myeloma Forum
database, we recently found that switching the previous drugs to lenalidomide in the plateau phase may perform betterin terms of OS compared with switching in non-plateau phase. These observations strongly suggest that in practical
medicine, it may be important to manage the plateau phase with continuous therapy. Furthermore, if physically possible,
there may be advantages to modifying the therapy in plateau phase in order to further reduce the tumor burden.

ランチョンセミナー179

ランチョンセミナー（Luncheon seminar）

LS3

Unmet medical needs in maintenance treatment for newly diagnosed multiple myeloma(NDMM)

Wee Joo Chng
National University Cancer Institute, Singapore (NCIS)

The use of maintenance therapy have been shown in a number of randomised clinical trials to improve progression freesurvival compared to placebo but it is not always clear that overall survival is improved. However a number of questions
remain open and controversial. What is the best agent or combination for maintenance, how long should maintenance be,does maintenance benefit all patients, as there are cost and toxicity implications, what is the true value of maintenance forpatients. At present, there are no clear answers to many of these questions but some recently developments may provide
a framework towards providing some answers.

180

ランチョンセミナー（Luncheon seminar）

LS4
三原

CD38 の基礎知識を骨髄腫治療に応用する ～ダラツムマブの効果を最大限に発揮するために～
Apply required knowledge about CD38 for treatment in myeloma patients～ To maximize the power of daratumumab for treatment ～圭一朗

Keichiro Mihara

広島大学病院 造血器診療科 血液内科

Department of Hematology, Hiroshima University Hospital, Japan

CD38 is a type II transmembrane glycoprotein and functions in a dimeric form. CD38 produces cADPR and NAADP,
which are associated with Ca signaling, cell adhesion, and signal transduction. CD38 is largely regulated by cytokines
involved in inflammation. Notably, it is of great interest that all trans-retinoic acid as well as interferon enhance CD38
expression on cell surface to most physicians and researchers. CD38 mRNA expression profiling shows that CD38mRNA is restrictedly expressed in blood cells, thymus, and prostate. However, it is of extreme important that several
evidences indicate CD38-null mice never elicit embryonic lethality and altered blood differentiation. Accordingly,
CD38 is determined not to be required for life nor hematopoiesis. Besides, mice lacking CD38 represent autism andshort-term depression, leading to CD38 being a multifunctional molecule, not a lineage marker. Myeloma cells strongly
express CD38, which is a most reliable marker as well as a most fascinated molecule for targeting therapy. During a last
couple years since FDA approved, anti-CD38 monoclonal antibody (daratumumab, DARA) has been striking impact on
myeloma treatment. POLLUX study showed over 90% of ORR and 58% of 30-months PFS with DARA in combination
with lenalidomide (R) and dexamethasone (d) (DRd) in patients with relapsed/ refractory myeloma. Accordingly, DARA
has been positioned as mainstay for myeloma therapy. Acquisition of knowledge about mode of action of DARA and agrounding in CD38 are required to maximize the power of DARA for treatment.

ランチョンセミナー

181

モーニングセミナー（Morning seminar）

MS1
伊藤

カルフィルゾミブの持つ免疫学特性＝長期使用が可能なプロテアソーム阻害薬＝
Focus on immunological characteristics behind Calfilzomib

量基

Tomoki Ito

関西医科大学附属病院 血液腫瘍内科

Kansai Medical University Hospital, Japan

Carfilzomib (CARF), a selective proteasome inhibitor (PI), has a strong antitumor activity in patients with multiple
myeloma (MM). Clinical pharmacokinetics of CARF is different from other PIs such as bortezomib or ixazomib. The
systemic half-life of CARF is very short (around 30 min); namely plasma concentration of CARF rapidly declines andreaches a plateau at low concentration in a biphasic manner after intravenous administration. Immunomodulatory effectsof CARF is considered to be negatively regulated similarly to bortezomib. There are no reports showing its effects onhuman dendritic cells (DCs), which are master cells in orchestrating both innate and acquire immune responses in a hostdefense. Human plasmacytoid DCs (pDCs) dedicate a large proportion of their transcription machinery to making type I
interferons (IFNs) and are the major source of IFN-α in the blood, which have the potential to enhance immune effectors
such as T cells, B cells, monocytes, and NK cells. Thus, pDCs play a central role in antiviral and antitumor immune
response. Here, we focus on and discuss the immunological characteristics of CARF from a view of the IFN-producing
capacity of human pDCs. The short duration of clinical CARF peak-concentration potentially provoke the IFN-producing
capacity of pDCs. The findings suggest a therapeutic ability of CARF without preventing the DC function. Therefore,
CARF has the potential effective as a continuous therapy without immunosuppression.

182

モーニングセミナー（Morning seminar）

MS2
萩原

多発性骨髄腫に対する免疫学的アプローチ
Immunological Approach for Multiple Myeloma將太郎

Shotaro Hagiwara

東京女子医科大学 血液内科学講座

Tokyo Women's Medical University, Department of Hematology, Japan

Multiple myeloma is an intractable hematologic malignancy, and the cause of its refractory nature is still not fully
understood.The recent advance of novel agents improves the therapeutic response and survival of newly diagnosed
and recurrent cases of multiple myeloma. Also, treatment after remission induction therapy including hematopoietic
stem cell transplantation and maintenance therapy contributes to the improvement of PFS. Nevertheless, a strategy tocure multiple myeloma has not been established. Anti-tumor immunity plays a crucial role in the suppression of thetumorigenesis and the progression. However, multiple myeloma cells have a shrewd mechanism to escape from thisantitumor immune system.The action of immune evasion includes the alteration of the phenotype of myeloma cells,
recruitment of immunosuppressive cells, releasing immune suppressive humoral factors.Myeloma cells can dodge
cellular immunity by increasing or decreasing the expression of antigens on the cell surface. Also, they induce theexpression of PD-1 in cytotoxic T cells and NK cells and PDL-1 on their cell surface. It can attenuate cytotoxicity
by effector cells. In the hypoxic environment, myeloma cells become dormant and resistant to apoptosis. In addition,
myeloid-derived suppressor cells in the bone marrow microenvironment impair the function of cytotoxic T cells and NK
cells.It has also been suggested that soluble MICA, soluble SLAMF 7, soluble CD 138, soluble BCMA may associatewith immunosuppression and myeloma progression.
Further investigation of strategies to eradicate myeloma cells by overcoming the immune evasion mechanisms is needed.

モーニングセミナー

183

スポンサードシンポジウム（Sponsored symposium）

SS1-1
半田

高齢多発性骨髄腫患者の治療 - 最適な治療を選択するために考慮すべきこと
Treatment for elderly multiple myeloma patients-What we evaluate for optimizing therapy?

寛

Hiroshi Handa

群馬大学大学院医学系研究科 内科学講座 血液内科学分野

Department of Hematology, Gunma University Graduate School of Medicine

Prognosis of multiple myeloma (MM) patient is rapidly improving by development of treatment including novel agents,
however survival of the elderly patients has not been adequately extended. Elderly patients were various compare toyoung patients, and frail elderly patient does not usually participate in clinical trials, thus knowledge for developing
optimal treatment is not sufficient. Prognosis of MM depends on staging, genetic and cytogenetic abnormalities.
However, general condition, organ function, comorbidities, daily life also impact on the prognosis, therefore evaluating
patient factors is important to optimize therapy. Early discontinuation of therapy due to adverse events (AE) associateswith shorter survival. Multi-comorbidity which potentially affects AE occurrence is common. Several comorbidity index
such as Charlson comorbidity index (CCI) or HCT-CI has been shown to be useful. Recently, comorbidity index easierand more specialized to MM patients namely myeloma Comorbidity Index (MCI) comprised of renal function, lungfunction, KPS, age and frailty was developed. IMWG constructed geriatric assessment (GA) tool using age, ADL, IADL
and CCI, and categorized elderly patients to three groups namely Fit, Intermediate Fitness and Frail. Both IMWG-GA
and MCI are useful to predict patients’ survival and may be useful for decision making. In this session, I am presenting
frailty scoring system and also case study to discuss how to assess and treat elderly patients. Continuing effort to
optimize treatment is important in our rapidly aging society.

184スポンサードシンポジウム（Sponsored symposium）

SS1-2

Emerging treatment options for elderly patients with multiple myeloma

Andrew Spencer
Professor, Department of Clinical Haematology, Alfred Hospital and Monash University

The treatment of multiple myeloma (MM) has evolved to be predicated largely on the utilisation of proteasome inhibitors(PI) (predominantly bortezomib) and immunomodulators (IMIDS) (mainly thalidomide and lenalidomide, but withsignificant geographical variation to access). Now superimposed on this PI-IMID framework are a range of immuneoncological (IO) agents that have demonstrated high levels of efficacy and the prospective of deeper and more durable
disease responses. Against this background the major challenge in translating these developments into meaningful benefit
for most patients is heterogeneity in disease biology and, in particular, the disease demography that reflects the advanced
age of most patients with newly diagnosed (transplant ineligible newly diagnosed MM – TI NDMM) and relapsed/refractory MM (RRMM). While a small number of pivotal studies have addressed the treatment of TI NDMM, studies
in RRMM remain ‘undifferentiated’ making no concession in terms of recruitment based on age or disease biology.
Real-world data from Australia and New Zealand (ANZ), the EU and US demonstrate that treatment duration at firstline, and even more so in the relapse setting, is significantly shorter that that demonstrated in clinical trials and that thisis even more of an issue in frail elderly patients. Moreover, this attenuation of treatment is likely a major contributor to
the inferior real-world survival of TI NDMM in comparison to clinical trial cohorts. Randomised studies of the CD38
targeting monoclonal antibody daratumumab (DZX) in RRMM demonstrate striking efficacy with the capacity to induced
MRD negativity. Importantly, DZX also demonstrates a highly favourable toxicity profile with comparable deliverability
to both young and elderly MM patients supporting the addition of DZX of standard-of-care regimens for elderly MM.

スポンサードシンポジウム

185

スポンサードシンポジウム（Sponsored symposium）

SS1-3

Assessing frailty in older MM patients

Saad Z. Usmani
Clinical Professor of Medicine, UNC School of Medicine, Levine Cancer Institute, Charlotte, NC“Multiple myeloma (MM) is the second most common hematologic malignancy in the world, diagnosed at a medianage of 70 years. Majority of MM patients are older and deemed transplant ineligible, on account of performance status
coupled with multiple co-morbidities. As the treatment landscape of MM is evolving with the introduction of new oral
agents and monoclonal antibodies, it is important to appreciate the need to assess frailty in older MM patients beyond
simply looking at performance status scales. The current presentation will cover available data on assessing frailty inolder MM patients. The presentation will also discuss data from several randomized phase III trials (SWOG-0777,
FIRST, ALCYONE, MAIA, Keynote-185, etc.) in light of the disease staging and the patient frailty perspective. Practicalguidelines of managing the older MM patients will also be discussed in light of all this information, as well as theupcoming clinical trials in this area.”186

スポンサードシンポジウム（Sponsored symposium）

SS2-1

Impact of Sustained Minimal Residual Disease (MRD) Negativity in Multiple Myeloma

Hervé Avet-Loiseau
Unite de Genomique du Myelome, CHU Rangueil, Toulouse, France

Multiple myeloma treatment has benefited from the introduction of novel treatment, improvements in supportive care,better understanding of disease biology, better diagnostic method, and new sensitive and specific tools for diseaseprognostication and management.
Especially, with the introduction of novel treatments such as IMiDs and Proteasome inhibitor for multiple myeloma,
patients are now achieving deeper and durable clinical responses. Recent studies have demonstrated that achieving
Minimal Residual Disease (MRD) negativity leads to better progression-free survival and overall survival outcomes.
Therefore, next-generation flow and sequencing methods to measure MRD in bone marrow are in use and being
developed with sensitivities in the range of 10−5 to 10−6 cells. These technologies may be combined with functional
imaging to detect MRD outside of bone marrow. Furthermore, to shorten evaluation times for new treatments, healthagencies are currently examining MRD as a surrogate end point in clinical trials. In the near future, MRD could be used
as a prognostic factor for making treatment decisions and for informing timing of therapeutic interventions.

スポンサードシンポジウム

187

スポンサードシンポジウム（Sponsored symposium）

SS2-2
髙松

日本国内における多発性骨髄腫 MRD 測定の現状
Minimal Residual Disease Assessment in Myeloma in Japan博幸

Hiroyuki Takamatsu

金沢大学医薬保健研究域医学系 血液内科

Department of Hematology, Faculty of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa
University, JapanThe complete response (CR) rate in multiple myeloma (MM) has increased owing to the development of novel agents,
and a good correlation between the CR rate and progression-free survival has been established. Therefore, new methods
to stratify CR cases based on the minimal residual disease (MRD) levels are needed to predict the prognosis of MM.
Multiparameter flow cytometry (MFC) has been used to assess MRD because of its rapidness in obtaining the results andthe high availability of patients with MM. EuroFlow-next generation flow has been developed for highly sensitive andstandardized detection of MRD in MM (Flores-Montero et al, Leukemia 2017). However, the procedure is expensive
to perform under the current Japanese public medical insurance system. Recently, two Japanese clinical laboratory
test companies, SRL and BML, have developed new inexpensive 8-color and 10-color single tube MFC methods,
respectively, to assess MRD in bone marrow under the current Japanese public medical insurance system. This lecture
will present the results of clinical trials for MM using MRD and the latest updates on MRD monitoring in Japan.

188

次回学術集会のご案内

会長

服部豊（慶應義塾大学 大学院薬学研究科 病態生理学）〒 105-8512 東京都港区芝公園 1-5-30

会期2020 年 5 月 16 日（土）、17 日（日）会場

浜松町コンベンションホール

〒 105-0013 東京都港区浜松町二丁目 3 番 1 号
TEL：03-6432-4075

日本生命浜松町クレアタワー 5・6F

運営事務局

日本コンベンションサービス株式会社〒 100-0013 東京都千代田区霞が関 1-4-2
TEL：03-3508-1214

大同生命霞が関ビル 14 階

FAX：03-3508-1302

E-mail：45jsm@convention.co.jp

会長からの一言
このプログラムが皆様のお手元に届くときには、新緑の心地よい季節が訪れていることと思います。この度は、第45 回日本骨髄腫学会学術集会を開催させていただけることとなり、大変光栄に存じております。ボルテゾミブやレナリドミド以降も新規薬剤が次々と登場し、骨髄腫患者の生存期間は著しく延長したことは誰もが認めるところと思います。その一方で、いかなる治療法にも抵抗性を示す症例、髄外病変を形成する症例、臓器障害によって十分に治療が施せない症例など、一向に予後が改善しない患者群が存在することも事実です。本学術集会では、このような「骨髄腫治療の限界の打破

新たな視点から病態を見つめて」をテーマとして、まず既存の治療方法をどのようなコンビ

ネーションでどのようなタイミングで使用するのが生存期間の延長につながるのかについて、情報交換してゆく必要があります。とくに、ボルテゾミブやレナリドミド以降の薬剤を早期に使用することの有用性、治療はいつ始めいつ終了するべきかは重要ポイントと思われます。さらに、治療抵抗例における生物学的アプローチあるいはゲノム解析
による病態解明と病勢モニタリング、その克服のための創薬研究についても検討してゆきたいと思います。また、症例ごとあるいは同一症例内でも多様なクローンが存在し、クローンが異なれば臨床像も異なる骨髄腫のダイバーシ
ティーにどのように立ち向かうかについて、臨床試験、バイオ、ゲノム、薬学といった様々な視点から考察を加えることができればと思います。

学会の二ヶ月後には東京オリンピックが開催され、日本が益々活気付いてまいります。骨髄腫治療もまた益々発展を来し、ハイリスクと呼ばれる患者さんも QOL を保ちながら天命を全うできるように我々は何をすべきか、熱い議論をいたしましょう。

189

過去の学術集会一覧

第 43 回

第 42 回

2018. 5. 12-13 東京ベイ幕張ホール（千葉県千葉市）中世古知昭「さらなる新しい時代の幕開け」
2017. 5. 27-28 ‌日本赤十字看護大学

広尾キャンパス ( 東京都渋谷区 ) 石田禎夫「治療を目指した骨髄腫研究の発展と治療の進歩」

第 41 回

2016. 5. 28-29 あわぎんホール（徳島県徳島市）安倍正博「骨髄腫研究の深化とさらなる治療の展開」

第 39 回2014. 5. 17-18 掛川グランドホテル（静岡県掛川市）名倉英一「骨髄腫治療の the State of the Art を考える」

第 40 回
第 38 回

2015. 5. 16-17 くまもと森都心プラザ（熊本県熊本市）畑裕之「内科学から見た骨髄腫」

2013. 7. 27 名古屋ルーセントタワー（愛知県名古屋市）清水一之

IMW2013 Kyoto 2013. 4. 3-7 国立京都国際会館（京都府京都市）清水一之

第 37 回

第 36 回

2012. 7. 7-8 ‌京都テルサ（京都府民総合交流プラザ内）（京都府京都市）島崎千尋「骨髄腫診療の原点を見つめ、未来を拓く」

2011. 11. 12-13 東京コンファレンスセンター（東京都港区）三輪哲義

第 35 回

2010. 11. 20-21 富山国際会議場（富山県富山市）吉田

第 33 回2008. 11. 15 広島大学医学部 広仁会館（広島県広島市）麻奥英毅

第 34 回
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第 11 回
第 10 回喬2009. 11. 21-22 新潟コンベンションセンター、朱鷺メッセ

2007. 11. 10 日本赤十字看護大学 広尾ホール（東京都渋谷区）鈴木憲史
2006. 11. 11 伊香保温泉 ホテル天坊（群馬県渋川市）村上博和

2005. 11. 12 京都府立医科大学付属図書館ホール（京都府京都市）谷脇雅史
2004. 11. 13 名古屋市中小企業振興会館（愛知県名古屋市）清水一之
2003. 10. 04 ロイトン札幌（北海道札幌市）今井浩三

2002. 11. 16 セミナーハウスクロス・ウェーブ（千葉県船橋市）高木敏之
2001. 10. 27 山口大学医学部霜仁会（山口県宇部市）河野道生
2000. 11. 18 国立国際医療センター（東京都新宿区）戸川1999. 11. 20 京都パークホテル（京都府京都市）加納

1998. 10. 17 札幌プリンスホテル北海道札幌市）三國主税
1997. 11. 29 虎ノ門パストラル（東京都港区）川戸正文
1996. 11. 30 徳島東急イン（徳島県徳島市）小阪昌明

1995. 11. 25 マーキュリーホール（群馬県前橋市）土屋1993. 12. 03 東京ガーデンパレスホテル（東京都文京区）高月1992. 01. 10 東京ガーデンパレスホテル（東京都文京区）今村幸雄
1990. 12. 14 東京ガーデンパレスホテル（東京都文京区）今村幸雄
1989. 12. 15 東京ガーデンパレスホテル（東京都文京区）今村幸雄
1989. 06. 23 新神戸オリエンタルホテル（兵庫県神戸市）磯部

第 3 回
第 2 回
第 1 回

190

敬

1988. 11. 18 東京ガーデンパレスホテル（東京都文京区）今村幸雄
1987. 12. 04 銀座東急ホテル（東京都中央区）今村幸雄

1987. 07. 24 ホテルギンモンド東京（東京都中央区）今村幸雄

1984. 11. 29 パレスホテル（東京都千代田区）今村幸雄

第 4 回

清

1992. 12. 04 東京ガーデンパレスホテル（東京都文京区）今村幸雄

第 7 回
第 5 回

純

1994. 12. 03 岡山プラザホテル（岡山県岡山市）瀬崎達雄

1986. 12. 05 全共連ビル（東京都千代田区）今村幸雄

第 6 回

敦

正

第 9 回
第 8 回

スノーホール（新潟県新潟市）張1985. 11. 29 キャピトル東急ホテル（東京都千代田区）今村幸雄
1984. 06. 27 キャピトル東急ホテル（東京都千代田区）今村幸雄

1984. 01. 20 住友三角ビル ･ 住友クラブ（東京都新宿区）今村幸雄
1983. 06. 24 住友三角ビル ･ 住友クラブ（東京都新宿区）今村幸雄
1981. 11. 19 住友三角ビル ･ 住友クラブ（東京都新宿区）今村幸雄
1981. 11. 18 住友三角ビル ･ 住友クラブ（東京都新宿区）今村幸雄
1980. 06. 04 パレスホテル（東京都千代田区）今村幸雄

高明

協賛企業一覧

第 44 回日本骨髄腫学会学術集会の開催にあたり、以下の企業・団体様のご協賛、ご協力をいただきました。
ここに深甚なる感謝の意を表します。
■共催セミナー

小野薬品工業株式会社
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ブリストル・マイヤーズ スクイブ株式会社
ヤンセンファーマ株式会社■企業展示

株式会社医学生物学研究所
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50 音順
2019 年 3 月 31 日現在
191

MEMO

MEMO

International Journal of Myeloma 2019, 9（1）International Journal of Myeloma 2019,（9 ）1 

日本骨髄腫学会誌

International Journal of Myeloma

個性に基づく骨髄腫治療時代の幕開け

プログラム・抄録集

第四十四回
日本骨髄腫学会学術集会
プログラム・抄録集

会期

会場
会長