bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Figure 5 from A Prime-Boost Vaccination Approach Induces Lung Resident Memory CD8+ T Cells Derived from Central Memory T Cells That Prevent Tumor Lung Metastasis
Authors: Xu Haoran , Yue Ming , Zhou Runhong , Wang Pui , Wong Michael Yik-Chun , Wang Jinlin , Huang Huarong , Chen Bohao , Mo Yufei , Tam Rachel Chun-Yee , Zhou Biao , Du Zhenglong , Huang Haode , Liu Li , Tan Zhiwu , Yuen Kwok-Yung , Song Youqiang , Chen Honglin , Chen Zhiwei
Published: October 2024

Antigen non-specific T cell response induced by V1 vaccination at day 30 post different T cell depletion
Figure S4 from Multidimensional Fragmentomics Enables Early and Accurate Detection of Colorectal Cancer
Authors: Cao Yuepeng , Wang Nannan , Wu Xuxiaochen , Tang Wanxiangfu , Bao Hua , Si Chengshuai , Shao Peng , Li Dongzheng , Zhou Xin , Zhu Dongqin , Yang Shanshan , Wang Fufeng , Su Guoqing , Wang Ke , Wang Qifan , Zhang Yao , Wang Qiangcheng , Yu Dongsheng , Jiang Qian , Bao Jun , Yang Liu
Published: October 2024

Figure S4
Figure S2 from Multidimensional Fragmentomics Enables Early and Accurate Detection of Colorectal Cancer
Authors: Cao Yuepeng , Wang Nannan , Wu Xuxiaochen , Tang Wanxiangfu , Bao Hua , Si Chengshuai , Shao Peng , Li Dongzheng , Zhou Xin , Zhu Dongqin , Yang Shanshan , Wang Fufeng , Su Guoqing , Wang Ke , Wang Qifan , Zhang Yao , Wang Qiangcheng , Yu Dongsheng , Jiang Qian , Bao Jun , Yang Liu
Published: October 2024

Figure S2
Table S1-S3 from NAT10 Phase Separation Regulates YTHDF1 Splicing to Promote Gastric Cancer Progression
Authors: Liu Songyi , Lin Chunlin , Lin Xiang , Lin Penghang , He Ruofan , Pan Xiaoyu , Lin Yan , Ye Jianxin , Zhu Guangwei
Published: October 2024

Supplementary Tables
Supplementary Figures S1–S10 from CCN6 Suppresses Metaplastic Breast Carcinoma by Antagonizing Wnt/β-Catenin Signaling to Inhibit EZH2-Driven EMT
Authors: Gonzalez Maria E. , Brophy Bryce , Eido Ahmad , Leonetti Adele E. , Djomehri Sabra I. , Augimeri Giuseppina , Carruthers Nicholas J. , Cavalcante Raymond G. , Giordano Francesca , Andò Sebastiano , Nesvizhskii Alexey I. , Fearon Eric R. , Kleer Celina G.
Published: October 2024

Suppl Figs S1–S10
Supplementary Data from AFDN Deficiency Promotes Liver Tropism of Metastatic Colorectal Cancer
Authors: Liao Shaoxia , Deng Jingwen , Deng Mengli , Chen Chaoyi , Han Fengyan , Ye Kehong , Wu Chenxia , Pan Lvyuan , Lai Maode , Tang Zhe , Zhang Honghe
Published: October 2024

Table S1. Information on the sequences of shRNAs, sgRNAs, and siRNAs;Table S2. Information of sequences for primers; Table S3. Information of primary antibodies;Figure S1. Expression levels of AFDN in the GEO database; Figure S2. AFDN deficiency promotes CRC cells migration and invasion; Figure S3. Snail knockdown did not reduce CRC cells migration and invasion induced by AFDN deficiency; Figure S4. CXCR4 expression was increased in AFDN-deficient cells.
Table S7 from Hypoxic Memory Mediates Prolonged Tumor-Intrinsic Type I Interferon Suppression to Promote Breast Cancer Progression
Authors: Iriondo Oihana , Mecenas Desirea , Li Yilin , Chin Christopher R. , Thomas Amal , Moriarty Aidan , Marker Rebecca , Wang Yiru J. , Hendrick Haley , Amzaleg Yonatan , Ortiz Veronica , MacKay Matthew , Dickerson Amber , Lee Grace , Harotoonian Sevana , Benayoun Bérénice A. , Smith Andrew , Mason Christopher E. , Roussos Torres Evanthia T. , Klotz Remi , Yu Min
Published: October 2024

Genes belonging to the hypoxia and IFN/AP signatures
Table S5 from Hypoxic Memory Mediates Prolonged Tumor-Intrinsic Type I Interferon Suppression to Promote Breast Cancer Progression
Authors: Iriondo Oihana , Mecenas Desirea , Li Yilin , Chin Christopher R. , Thomas Amal , Moriarty Aidan , Marker Rebecca , Wang Yiru J. , Hendrick Haley , Amzaleg Yonatan , Ortiz Veronica , MacKay Matthew , Dickerson Amber , Lee Grace , Harotoonian Sevana , Benayoun Bérénice A. , Smith Andrew , Mason Christopher E. , Roussos Torres Evanthia T. , Klotz Remi , Yu Min
Published: October 2024

GSEA analysis with genes upregulated in responders compared to non-responders
Figure S3 from Hypoxic Memory Mediates Prolonged Tumor-Intrinsic Type I Interferon Suppression to Promote Breast Cancer Progression
Authors: Iriondo Oihana , Mecenas Desirea , Li Yilin , Chin Christopher R. , Thomas Amal , Moriarty Aidan , Marker Rebecca , Wang Yiru J. , Hendrick Haley , Amzaleg Yonatan , Ortiz Veronica , MacKay Matthew , Dickerson Amber , Lee Grace , Harotoonian Sevana , Benayoun Bérénice A. , Smith Andrew , Mason Christopher E. , Roussos Torres Evanthia T. , Klotz Remi , Yu Min
Published: October 2024

Hypoxia suppression of IFN/AP lasts longer than the hypoxic exposure
Data from Induced Pluripotent Stem Cells Facilitate the Development and Evaluation of Cancer Vaccines
Authors: Zhai Yuewen , Xu Xinyu , Fang Ji , He Fang , Li Siwen
Published: October 2024

Abstract
Cancer vaccines are an approach to elicit amplified antigen-specific immune responses. Induced pluripotent stem cells (iPSC) have potential utility for the development of universal vaccines because of their intrinsic antigenic epitopes. Concurrently, iPSCs can undergo pluripotent differentiation and are thus a stable source of both antigen-presenting cells for producing immune cell-based vaccines and tumor organoids for facilitating the exploration and adaptive assessment of tumor vaccines. This review describes the specific contributions of iPSCs to vaccine development, summarizes their diverse developmental trajectories, and discusses the obstacles to their application along with potential solutions.
Data from Therapeutic Targeting of the GLS1–c-Myc Positive Feedback Loop Suppresses Glutaminolysis and Inhibits Progression of Head and Neck Cancer
Authors: Yang Jianqiang , Chen Fanghui , Lang Liwei , Yang Fan , Fu Zhenzhen , Martinez Juan , Cho Amber , Saba Nabil F. , Teng Yong
Published: October 2024

Abstract
Head and neck squamous cell carcinoma (HNSCC) is addicted to glutaminolysis. Targeting this metabolic dependency has emerged as a potential therapeutic approach for HNSCC. In this study, we conducted a bioinformatic analysis of The Cancer Genome Atlas HNSCC cohort that revealed a robust correlation between expression of MYC (encoding the protein c-Myc) and glutaminase 1 (GLS1), which catalyzes the first step in glutaminolysis. Intriguingly, disruption of GLS1 signaling in HNSCC cells by genetic depletion or CB-839 treatment resulted in a reduction in c-Myc protein stability via a ubiquitin-specific peptidase 1–dependent ubiquitin–proteasome pathway. On the other hand, c-Myc directly binds to the promoter region of GLS1 and upregulates its transcription. Notably, the GLS1–c-Myc pathway enhanced acetyl-coenzyme A carboxylase–dependent Slug acetylation, prompting cancer cell invasion and metastasis. Thus, the GLS1–c-Myc axis emerged as a positive feedback loop critical for driving the aggressiveness of HNSCC. Therapeutically, combining CB-839 with the c-Myc inhibitor MYCi975 strongly suppressed GLS1–c-Myc signaling, resulting in a superior antitumor effect compared with either single agent in an orthotopic mouse model of HNSCC. These findings hold promise for the development of effective therapies for patients with HNSCC, addressing an urgent need arising from the significant incidence and high metastatic rate of the disease.

Significance: GLS1 and c-Myc form a positive feedback loop that promotes head and neck cancer metastasis and can be targeted as a promising therapeutic strategy for this disease.
Data from CCN6 Suppresses Metaplastic Breast Carcinoma by Antagonizing Wnt/β-Catenin Signaling to Inhibit EZH2-Driven EMT
Authors: Gonzalez Maria E. , Brophy Bryce , Eido Ahmad , Leonetti Adele E. , Djomehri Sabra I. , Augimeri Giuseppina , Carruthers Nicholas J. , Cavalcante Raymond G. , Giordano Francesca , Andò Sebastiano , Nesvizhskii Alexey I. , Fearon Eric R. , Kleer Celina G.
Published: October 2024

Abstract
Metaplastic breast carcinomas (mBrCA) are a highly aggressive subtype of triple-negative breast cancer with histologic evidence of epithelial-to-mesenchymal transition and aberrant differentiation. Inactivation of the tumor suppressor gene cellular communication network factor 6 (CCN6; also known as Wnt1-induced secreted protein 3) is a feature of mBrCAs, and mice with conditional inactivation of Ccn6 in mammary epithelium (Ccn6-KO) develop spindle mBrCAs with epithelial-to-mesenchymal transition. Elucidation of the precise mechanistic details of how CCN6 acts as a tumor suppressor in mBrCA could help identify improved treatment strategies. In this study, we showed that CCN6 interacts with the Wnt receptor FZD8 and coreceptor LRP6 on mBrCA cells to antagonize Wnt-induced activation of β-catenin/TCF-mediated transcription. The histone methyltransferase EZH2 was identified as a β-catenin/TCF transcriptional target in Ccn6-KO mBrCA cells. Inhibiting Wnt/β-catenin/TCF signaling in Ccn6-KO mBrCA cells led to reduced EZH2 expression, decreased histone H3 lysine 27 trimethylation, and deregulation of specific target genes. Pharmacologic inhibition of EZH2 reduced growth and metastasis of Ccn6-KO mBrCA mammary tumors in vivo. Low CCN6 is significantly associated with activated β-catenin and high EZH2 in human spindle mBrCAs compared with other subtypes. Collectively, these findings establish CCN6 as a key negative regulator of a β-catenin/TCF/EZH2 axis and highlight the inhibition of β-catenin or EZH2 as a potential therapeutic approach for patients with spindle mBrCAs.

 Significance: CCN6 deficiency drives metaplastic breast carcinoma growth and metastasis by increasing Wnt/β-catenin activation to upregulate EZH2, identifying EZH2 inhibition as a mechanistically guided treatment strategy for this deadly form of breast cancer.
Supplementary Figure S8 from Targeting the Dendritic Cell-Secreted Immunoregulatory Cytokine CCL22 Alleviates Radioresistance
Authors: Bugno Jason , Wang Liangliang , Yu Xianbin , Cao Xuezhi , Wang Jiaai , Huang Xiaona , Yang Kaiting , Piffko Andras , Chen Katherine , Luo Stephen Y. , Naccasha Emile , Hou Yuzhu , Fu Sherry , He Chuan , Fu Yang-xin , Liang Hua L. , Weichselbaum Ralph R.
Published: October 2024

Supplementary Figure S8. Bulk RNA-sequencing of tumor myeloid cells 7 days after RT and αEGFR-IFNα
Supplementary Figure S10 from Targeting the Dendritic Cell-Secreted Immunoregulatory Cytokine CCL22 Alleviates Radioresistance
Authors: Bugno Jason , Wang Liangliang , Yu Xianbin , Cao Xuezhi , Wang Jiaai , Huang Xiaona , Yang Kaiting , Piffko Andras , Chen Katherine , Luo Stephen Y. , Naccasha Emile , Hou Yuzhu , Fu Sherry , He Chuan , Fu Yang-xin , Liang Hua L. , Weichselbaum Ralph R.
Published: October 2024

Supplementary Figure S10. αEGFR-IFNα enhances radiation efficacy in part through CD8+ T cells
Supplementary Figure S8 from Spatial Transcriptome Mapping of the Desmoplastic Growth Pattern of Colorectal Liver Metastases by In Situ Sequencing Reveals a Biologically Relevant Zonation of the Desmoplastic Rim
Authors: Andersson Axel , Escriva Conde Maria , Surova Olga , Vermeulen Peter , Wählby Carolina , Nilsson Mats , Nyström Hanna
Published: October 2024

Supplementary Figure S8. Identification of bile ducts in cluster 6. Cluster 6 marks bile ducts and is mainly driven by SPP1 expression. The scale bar corresponds to 200 μm.
Supplemental Table 4 from Abiraterone, Olaparib, or Abiraterone + Olaparib in First-Line Metastatic Castration-Resistant Prostate Cancer with DNA Repair Defects (BRCAAway)
Authors: Hussain Maha , Kocherginsky Masha , Agarwal Neeraj , Adra Nabil , Zhang Jingsong , Paller Channing J. , Picus Joel , Reichert Zachery R. , Szmulewitz Russell Z. , Tagawa Scott T. , Kuzel Timothy M. , Bazzi Latifa A. , Daignault-Newton Stephanie , Whang Young E. , Dreicer Robert , Stephenson Ryan D. , Rettig Matthew B. , Shevrin Daniel , Gerke Travis , Chinnaiyan Arul M. , Antonarakis Emmanuel S.
Published: October 2024

Supplemental Table 4. Patient Demographics.
Supplementary Figure S2 from Pharmacologic Inhibition of EIF4A Blocks NRF2 Synthesis to Prevent Osteosarcoma Metastasis
Authors: Lizardo Michael M. , Hughes Christopher , Huang Yue Z. , Shyp Taras , Delaidelli Alberto , Zhang Hai-Feng , Shaool Sol Snir , Renner Annalena F. , Burwag Farez , Sayles Leanne C. , Lee Alex G. , Sweet-Cordero Alejandro , Sorensen Poul H.
Published: October 2024

Fig. S2. CR-1-31B single agent activity in in vivo and ex vivo models of metastatic OS.
Supplementary Data S1 from Pharmacologic Inhibition of EIF4A Blocks NRF2 Synthesis to Prevent Osteosarcoma Metastasis
Authors: Lizardo Michael M. , Hughes Christopher , Huang Yue Z. , Shyp Taras , Delaidelli Alberto , Zhang Hai-Feng , Shaool Sol Snir , Renner Annalena F. , Burwag Farez , Sayles Leanne C. , Lee Alex G. , Sweet-Cordero Alejandro , Sorensen Poul H.
Published: October 2024

Supplementary Data file containing Supplementary Methods and Materials and associated references.
Supplementary Table 6 from Colorectal Cancer Recurrence Prediction Using a Tissue-Free Epigenomic Minimal Residual Disease Assay
Authors: Nakamura Yoshiaki , Tsukada Yuichiro , Matsuhashi Nobuhisa , Murano Tatsuro , Shiozawa Manabu , Takahashi Yusuke , Oki Eiji , Goto Masahiro , Kagawa Yoshinori , Kanazawa Akiyoshi , Ohta Takashi , Ouchi Akira , Bando Hideaki , Uchigata Hiroshi , Notake Chiemi , Ikematsu Hiroaki , Yoshino Takayuki
Published: October 2024

Supplementary Table 6. Risk of recurrence based on ctDNA detection following adjuvant chemotherapy in patients with stage II or higher CRC. Tables to accompany Figure 5A-B.
Supplementary Figure S1 from Tyrosine Protein Kinase SYK-Related Gene Signature in Baseline Immune Cells Associated with Adjuvant Immunotherapy–Induced Immune-Related Adverse Events in Melanoma
Authors: Monson Kelsey R. , Ferguson Robert , Handzlik Joanna E. , Xiong Jiahan , Dagayev Sasha , Morales Leah , Chat Vylyny , Bunis Anabelle , Sreenivasaiah Chaitra , Dolfi Sonia , Tenney Daniel J. , Shao Yongzhao , Osman Iman , Weber Jeffrey S. , Kirchhoff Tomas
Published: October 2024

Supplementary Figure S1. Sample size and power calculation for different effect size values.
Supplementary Figure 2 from Colorectal Cancer Recurrence Prediction Using a Tissue-Free Epigenomic Minimal Residual Disease Assay
Authors: Nakamura Yoshiaki , Tsukada Yuichiro , Matsuhashi Nobuhisa , Murano Tatsuro , Shiozawa Manabu , Takahashi Yusuke , Oki Eiji , Goto Masahiro , Kagawa Yoshinori , Kanazawa Akiyoshi , Ohta Takashi , Ouchi Akira , Bando Hideaki , Uchigata Hiroshi , Notake Chiemi , Ikematsu Hiroaki , Yoshino Takayuki
Published: October 2024

Supplementary Figure 2. Flow diagram of patient inclusion/exclusion criteria for analysis sets and sample disposition for the study population.
Supplementary Figure S2 from The Innate Immune Landscape of dMMR/MSI Cancers Predicts the Outcome of Nivolumab Treatment: Results from the Drug Rediscovery Protocol
Authors: Zeverijn Laurien J. , Geurts Birgit S. , Battaglia Thomas W. , van Berge Henegouwen Jade M. , de Wit Gijs F. , Hoes Louisa R. , van der Wijngaart Hanneke , van der Noort Vincent , Roepman Paul , de Leng Wendy W.J. , Jansen Anne M.L. , Chalabi Myriam , van Herpen Carla M.L. , Devriese Lot A. , Erdkamp Frans L.G. , Labots Mariette , de Jonge Maja J.A. , Kerver Emile D. , Bins Adriaan D. , Leek Lindsay V.M. , Notohardjo Jessica C.L. , van den Eertwegh Alfonsus J.M. , Wessels Lodewyk F.A. , Verheul Henk M.W. , Gelderblom Hans , van de Haar Joris , Voest Emile E.
Published: October 2024

Supplementary Figure S2. Genomic biomarkers of clinical benefit to ICB.
Supplementary Table S3 from Clinical Value of Liquid Biopsy in Patients with FGFR2 Fusion–Positive Cholangiocarcinoma During Targeted Therapy
Authors: González-Medina Alberto , Vila-Casadesús Maria , Gomez-Rey Marina , Fabregat-Franco Carles , Sierra Alexandre , Tian Tian V. , Castet Florian , Castillo Gloria , Matito Judit , Martinez Paola , Miquel Josep M. , Nuciforo Paolo , Pérez-López Raquel , Macarulla Teresa , Vivancos Ana
Published: October 2024

Supplementary Table S3. Clinicopathological characteristics of retrospective cohort patients.
Supplementary Figure S10 from Clinical Value of Liquid Biopsy in Patients with FGFR2 Fusion–Positive Cholangiocarcinoma During Targeted Therapy
Authors: González-Medina Alberto , Vila-Casadesús Maria , Gomez-Rey Marina , Fabregat-Franco Carles , Sierra Alexandre , Tian Tian V. , Castet Florian , Castillo Gloria , Matito Judit , Martinez Paola , Miquel Josep M. , Nuciforo Paolo , Pérez-López Raquel , Macarulla Teresa , Vivancos Ana
Published: October 2024

Supplementary Figure S10. Follow-up in plasma samples collected not periodically.
Supplementary Figure S1 from Clinical Value of Liquid Biopsy in Patients with FGFR2 Fusion–Positive Cholangiocarcinoma During Targeted Therapy
Authors: González-Medina Alberto , Vila-Casadesús Maria , Gomez-Rey Marina , Fabregat-Franco Carles , Sierra Alexandre , Tian Tian V. , Castet Florian , Castillo Gloria , Matito Judit , Martinez Paola , Miquel Josep M. , Nuciforo Paolo , Pérez-López Raquel , Macarulla Teresa , Vivancos Ana
Published: October 2024

Supplementary Figure S1. Validation of sWGS from off-targets reads for 32 samples.
Data from FDA Approval Summary: Asciminib for Ph+ CML in Chronic Phase Treated with Two or More Tyrosine Kinase Inhibitors and for the T315I Mutation
Authors: Pamuk Gulsum E. , Chow Edwin C.Y. , Ionan Alexei C. , Chen Haiyan , Lee Shwu-Luan , Hsu Vicky , Grimstein Manuela , Zheng Nan , Sun Jielin , Charlab Rosane , Gehrke Brenda J. , Vallejo Jonathon , Ehrlich Lori A. , de Claro R. Angelo , Theoret Marc R.
Published: October 2024

Abstract
On October 29, 2021, FDA granted accelerated approval to asciminib (SCEMBLIX; Novartis), a tyrosine kinase inhibitor (TKI), for the treatment of adult patients with Philadelphia chromosome positive chronic myeloid leukemia (Ph+ CML) in chronic phase (CP), previously treated with two or more TKIs, and granted traditional approval to asciminib for adult patients with Ph+ CML in CP with the T315I mutation. The first indication was approved based on major molecular response (MMR) at 24 weeks in the ASCEMBL study, a randomized trial comparing asciminib with bosutinib in patients who had failed two or more TKIs. This indication was ultimately granted traditional approval on October 12, 2022, based on safety data and MMR rate at 96 weeks of 38% [95% confidence interval (CI), 30–46] in the asciminib arm versus 16% (95% CI, 8–26) in the bosutinib arm (P value: 0.001). The second indication was approved based on MMR rate by 96 weeks of 49% (95% CI, 34–64) in the single-arm CABL001X2101 study. The most common (≥20%) adverse reactions included upper respiratory tract infections, musculoskeletal pain, headache, fatigue, nausea, rash, and diarrhea. The most common (≥20%) laboratory abnormalities were thrombocytopenia, neutropenia, anemia, lymphopenia, hypertriglyceridemia, hyperuricemia, and increases in creatine kinase, alanine aminotransferase, aspartate aminotransferase, lipase, and amylase. This manuscript describes the basis for approval of these indications.
Data from Clinical Value of Liquid Biopsy in Patients with FGFR2 Fusion–Positive Cholangiocarcinoma During Targeted Therapy
Authors: González-Medina Alberto , Vila-Casadesús Maria , Gomez-Rey Marina , Fabregat-Franco Carles , Sierra Alexandre , Tian Tian V. , Castet Florian , Castillo Gloria , Matito Judit , Martinez Paola , Miquel Josep M. , Nuciforo Paolo , Pérez-López Raquel , Macarulla Teresa , Vivancos Ana
Published: October 2024

AbstractPurpose:
FGFR2 fusions occur in 10% to 15% of patients with intrahepatic cholangiocarcinoma (iCCA), potentially benefiting from FGFR inhibitors (FGFRi). We aimed to assess the feasibility of detecting FGFR2 fusions in plasma and explore plasma biomarkers for managing FGFRi treatment.
Experimental Design:
We conducted a retrospective study in 18 patients with iCCA and known FGFR2 fusions previously identified in tissue samples from prior FGFRi treatment. Both tissue and synchronous plasma samples were analyzed using a custom hybrid capture gene panel with next-generation sequencing (VHIO-iCCA panel) and validated against commercial vendor results. Longitudinal plasma analysis during FGFRi was performed. Subsequently, we explored the correlation between plasma biomarkers, liver enzymes, tumor volume, and clinical outcomes.
Results:
Sixteen patients (88.9%) were positive for FGFR2 fusion events in plasma. Remarkably, the analysis of plasma suggests that lower levels of ctDNA are linked to clinical benefits from targeted therapy and result in improved progression-free survival and overall survival. Higher concentrations of cell-free DNA before FGFRi treatment were linked to worse overall survival, correlating with impaired liver function and indicating compromised cell-free DNA removal by the liver. Additionally, increased ctDNA or the emergence of resistance mutations allowed earlier detection of disease progression compared with standard radiologic imaging methods.
Conclusions:
VHIO-iCCA demonstrated accurate detection of FGFR2 fusions in plasma. The integration of information from various plasma biomarkers holds the potential to predict clinical outcomes and identify treatment failure prior to radiologic progression, offering valuable guidance for the clinical management of patients with iCCA.
Supplementary Figure S7 from Anti-Claudin-2 Antibody–Drug Conjugates for the Treatment of Colorectal Cancer Liver Metastasis
Authors: Tabariès Sébastien , Robert Alma , Marcil Anne , Ling Binbing , Acchione Mauro , Lippens Julie , Pagé Martine , Fortin Annie , Meury Luc , Coutu Mathieu , Annis Matthew G. , Girondel Charlotte , Navarre Julie , Jaramillo Maria , Moraitis Anna N. , Siegel Peter M.
Published: October 2024

Supplementary Figure S7
Supplementary Figure S1 from Anti-Claudin-2 Antibody–Drug Conjugates for the Treatment of Colorectal Cancer Liver Metastasis
Authors: Tabariès Sébastien , Robert Alma , Marcil Anne , Ling Binbing , Acchione Mauro , Lippens Julie , Pagé Martine , Fortin Annie , Meury Luc , Coutu Mathieu , Annis Matthew G. , Girondel Charlotte , Navarre Julie , Jaramillo Maria , Moraitis Anna N. , Siegel Peter M.
Published: October 2024

Supplementary Figure S1
Figure S8 from Characterization of AB598, a CD39 Enzymatic Inhibitory Antibody for the Treatment of Solid Tumors
Authors: Anderson Amy E. , Parashar Kaustubh , Jin Ke , Clor Julie , Stagnaro Carlo E. , Vani Urvi , Singh Jaskirat , Chen Ada , Guan Yihong , Talukdar Priyanka , Sathishkumar Pavithra , Juat Damie J. , Singh Hema , Kushwaha Ritu , Zhao Xiaoning , Kaplan Angelo , Seitz Lisa , Walters Matthew J. , Fernandez-Salas Ester , Walker Nigel P.C. , Bowman Christine E.
Published: October 2024

Figure S8
Figure S7 from PKMYT1 Is a Marker of Treatment Response and a Therapeutic Target for CDK4/6 Inhibitor-Resistance in ER+ Breast Cancer
Authors: Chen Anran , Kim Beom-Jun , Mitra Aparna , Vollert Craig T. , Lei Jonathan T. , Fandino Diana , Anurag Meenakshi , Holt Matthew V. , Gou Xuxu , Pilcher Jacob B. , Goetz Matthew P. , Northfelt Donald W. , Hilsenbeck Susan G. , Marshall C. Gary , Hyer Marc L. , Papp Robert , Yin Shou-Yun , De Angelis Carmine , Schiff Rachel , Fuqua Suzanne A.W. , Ma Cynthia X. , Foulds Charles E. , Ellis Matthew J.
Published: October 2024

MCF7 EDR Palbo-R cell line displays cross-resistance to two other CDK4/6 inhibitors, in addition to being palbociclib-resistant
Supplementary Figure S7 from Blocking M2-Like Macrophage Polarization Using Decoy Oligodeoxynucleotide-Based Gene Therapy Prevents Immune Evasion for Pancreatic Cancer Treatment
Authors: Chen Chang-Jung , Wang Hao-Chen , Hou Ya-Chin , Wu Yi-Ying , Shieh Chi-Chang , Shan Yan-Shen
Published: October 2024

Supplementary Figure S7. The interaction between HDAC2 and CYBB in U937 cells is stimulated by co-cultured with PANC-1 cells. RT-qPCR analysis of CYBB expression in U937 cells pretreated with inhibitors after co-culture with PANC-1 cells for 72h. The bar graphs depict relative mRNA expression. ***, p < 0.001, significant differences between groups. Data represent the mean of 3 independent experiments.
Supplementary Figure S15 from Blocking M2-Like Macrophage Polarization Using Decoy Oligodeoxynucleotide-Based Gene Therapy Prevents Immune Evasion for Pancreatic Cancer Treatment
Authors: Chen Chang-Jung , Wang Hao-Chen , Hou Ya-Chin , Wu Yi-Ying , Shieh Chi-Chang , Shan Yan-Shen
Published: October 2024

Supplementary Figure S15. The uncropped Western blot images in the main and supplementary figures are included.
Table S5 from AKT Inhibition Sensitizes to Polo-Like Kinase 1 Inhibitor Onvansertib in Prostate Cancer
Authors: Nouri Mannan , Varkaris Andreas , Ridinger Maya , Dalrymple Susan L. , Dennehy Christopher M. , Isaacs John T. , Einstein David J. , Brennen W.N. , Balk Steven P.
Published: October 2024

Table S5 (Selected Hits)
Supplementary Figure S7 from The SOS1 Inhibitor MRTX0902 Blocks KRAS Activation and Demonstrates Antitumor Activity in Cancers Dependent on KRAS Nucleotide Loading
Authors: Sudhakar Niranjan , Yan Larry , Qiryaqos Fadia , Engstrom Lars D. , Laguer Jade , Calinisan Andrew , Hebbert Allan , Waters Laura , Moya Krystal , Bowcut Vickie , Vegar Laura , Ketcham John M. , Ivetac Anthony , Smith Christopher R. , Lawson J. David , Rahbaek Lisa , Clarine Jeffrey , Nguyen Natalie , Saechao Barbara , Parker Cody , Elliott Adam J. , Vanderpool Darin , He Leo , Hover Laura D. , Fernandez-Banet Julio , Coma Silvia , Pachter Jonathan A. , Hallin Jill , Marx Matthew A. , Briere David M. , Christensen James G. , Olson Peter , Haling Jacob , Khare Shilpi
Published: October 2024

Supplementary Figure S7 shows the improved antiproliferative activity observed with the MRTX0902/avutometinib combination in KRAS-MAPK pathway mutant models, LN229 (PTPN11 A72S) and NCI-H1435 (NF1 K615N).
Data from FZ-AD005, a Novel DLL3-Targeted Antibody–Drug Conjugate with Topoisomerase I Inhibitor, Shows Potent Antitumor Activity in Preclinical Models
Authors: Guo Qingsong , Gao Bei , Song Ruiwen , Li Weinan , Zhu Shulei , Xie Qian , Lou Sensen , Wang Lei , Shen Jiafei , Zhao Teng , Zhang Yifan , Wu Jinsong , Lu Wei , Yang Tong
Published: October 2024

Abstract
Delta-like ligand 3 (DLL3) is overexpressed in small cell lung cancer (SCLC) and has been considered an attractive target for SCLC therapy. Rovalpituzumab tesirine was the first DLL3-targeted antibody–drug conjugate (ADC) to enter clinical studies. However, serious adverse events limited progress in the treatment of SCLC with rovalpituzumab tesirine. In this study, we developed a novel DLL3-targeted ADC, FZ-AD005, by using DXd with potent cytotoxicity and a relatively better safety profile to maximize the therapeutic index. FZ-AD005 was generated by a novel anti-DLL3 antibody, FZ-A038, and a valine–alanine (Val–Ala) dipeptide linker to conjugate DXd. Moreover, Fc-silencing technology was introduced in FZ-AD005 to avoid off-target toxicity mediated by FcγRs and showed negligible Fc-mediated effector functions in vitro. In preclinical evaluation, FZ-AD005 exhibited DLL3-specific binding and demonstrated efficient internalization, bystander killing, and excellent in vivo antitumor activities in cell line–derived xenograft and patient-derived xenograft models. FZ-AD005 was stable in circulation with acceptable pharmacokinetic profiles in cynomolgus monkeys. FZ-AD005 was well tolerated in rats and monkeys. The safety profile of FZ-AD005 was favorable, and the highest nonseverely toxic dose was 30 mg/kg in cynomolgus monkeys. In conclusion, FZ-AD005 has the potential to be a superior DLL3-targeted ADC with a wide therapeutic window and is expected to provide clinical benefits for the treatment of patients with SCLC.
Data from Discovery of Monovalent Direct Degraders of BRD4 that Act via the Recruitment of DCAF11
Authors: Parker Gregory S. , Toth Julia I. , Fish Sarah , Blanco Gabrielle , Kampert Taylor , Li Xiaoming , Yang Linette , Stumpf Craig R. , Steadman Kenneth , Jamborcic Aleksandar , Chien Stephen , Daniele Elizabeth , Dearie Alejandro , Leriche Geoffray , Bailey Simon , Thompson Peggy A.
Published: October 2024

Abstract
Targeted protein degradation (TPD) using the ubiquitin proteasome system (UPS) is a rapidly growing drug discovery modality to eliminate pathogenic proteins. Strategies for TPD have focused on heterobifunctional degraders that often suffer from poor drug-like properties, and molecular glues that rely on serendipitous discovery. Monovalent “direct” degraders represent an alternative approach, in which small molecules bind to a target protein and induce degradation of that protein through the recruitment of an E3 ligase complex. Using an ultra-high throughput cell-based screening platform, degraders of the bromodomain extraterminal protein BRD4 were identified and optimized to yield a lead compound, PLX-3618. In this paper, we demonstrate that PLX-3618 elicited UPS-mediated selective degradation of BRD4, resulting in potent antitumor activity in vitro and in vivo. Characterization of the degradation mechanism identified DCAF11 as the E3 ligase required for PLX-3618-mediated degradation of BRD4. Protein–protein interaction studies verified a BRD4:PLX-3618:DCAF11 ternary complex, and mutational studies provided further insights into the DCAF11-mediated degradation mechanism. Collectively, these results demonstrate the discovery and characterization of a novel small molecule that selectively degrades BRD4 through the recruitment of the E3 substrate receptor, DCAF11, and promotes potent antitumor activity in vivo.
Supplementary Figure S2 from Cancer History and Social Support Impact Colorectal Cancer Screening Utilization by Race/Ethnicity
Authors: Tsai Meng-Han , Lee Minjee , Coughlin Steven S. , Eberth Jan M. , Rogers Charles R.
Published: October 2024

Supplementary Figure S2 showed the association between race/ethnicity, cancer history, lack of social support, and CRC screening utilization
Figure S7 from NK Receptor Signaling Lowers TCR Activation Threshold, Enhancing Selective Recognition of Cancer Cells by TAA-Specific CTLs
Authors: Dong Bowen , Obermajer Nataša , Tsuji Takemasa , Matsuzaki Junko , Bonura Cindy M. , Sander Cindy , Withers Henry , Long Mark D. , Chavel Colin , Olejniczak Scott H. , Minderman Hans , Kirkwood John M. , Edwards Robert P. , Storkus Walter J. , Romero Pedro , Kalinski Pawel
Published: October 2024

Chemotherapeutic drugs elevate NKR-L expression on cancer cells.
Supplemental Table S17 from Machine Learning–Directed Conversion of Glioblastoma Cells to Dendritic Cell–Like Antigen-Presenting Cells as Cancer Immunotherapy
Authors: Liu Tianyi , Jin Dan , Le Son B. , Chen Dongjiang , Sebastian Mathew , Riva Alberto , Liu Ruixuan , Tran David D.
Published: October 2024

CFDs for human LN GBM → iDC-APC conversion (Support Main Figure 7)
Supplemental Table S12 from Machine Learning–Directed Conversion of Glioblastoma Cells to Dendritic Cell–Like Antigen-Presenting Cells as Cancer Immunotherapy
Authors: Liu Tianyi , Jin Dan , Le Son B. , Chen Dongjiang , Sebastian Mathew , Riva Alberto , Liu Ruixuan , Tran David D.
Published: October 2024

All public murine datasets curated for ML predictions (supporting Main Figure 1)
Supplemental Figure S5 from Machine Learning–Directed Conversion of Glioblastoma Cells to Dendritic Cell–Like Antigen-Presenting Cells as Cancer Immunotherapy
Authors: Liu Tianyi , Jin Dan , Le Son B. , Chen Dongjiang , Sebastian Mathew , Riva Alberto , Liu Ruixuan , Tran David D.
Published: October 2024

Conversion of murine GBM cells to iDC-APCs (Supporting Main Figure 1)
Supplemental Figure S19 from Machine Learning–Directed Conversion of Glioblastoma Cells to Dendritic Cell–Like Antigen-Presenting Cells as Cancer Immunotherapy
Authors: Liu Tianyi , Jin Dan , Le Son B. , Chen Dongjiang , Sebastian Mathew , Riva Alberto , Liu Ruixuan , Tran David D.
Published: October 2024

Expression of CFDs in human GBM cells. (Supporting Main Figure 7)
Supplemental Figure S17 from Machine Learning–Directed Conversion of Glioblastoma Cells to Dendritic Cell–Like Antigen-Presenting Cells as Cancer Immunotherapy
Authors: Liu Tianyi , Jin Dan , Le Son B. , Chen Dongjiang , Sebastian Mathew , Riva Alberto , Liu Ruixuan , Tran David D.
Published: October 2024

Human PU.1 + IKZF1 (hP-IKZF1 or PI) is 3-30-fold more efficient at inducing CD45+ and CD45+MHCII+ cells, respectively, compared to hP-ev alone. (Supporting Main Figure 7)
Supplemental Figure S11 from Machine Learning–Directed Conversion of Glioblastoma Cells to Dendritic Cell–Like Antigen-Presenting Cells as Cancer Immunotherapy
Authors: Liu Tianyi , Jin Dan , Le Son B. , Chen Dongjiang , Sebastian Mathew , Riva Alberto , Liu Ruixuan , Tran David D.
Published: October 2024

Murine iDCs-APCs lack B and T cell markers. (Supporting Main Figure 2A)
Table S3 from Hypoxia-Induced Long Noncoding RNA HIF1A-AS2 Regulates Stability of MHC Class I Protein in Head and Neck Cancer
Authors: Liao Tsai-Tsen , Chen Yu-Hsien , Li Zih-Yu , Hsiao An-Ching , Huang Ya-Li , Hao Ruo-Xin , Tai Shyh-Kuan , Chu Pen-Yuan , Shih Jing-Wen , Kung Hsing-Jien , Yang Muh-Hwa
Published: October 2024

Primary antibodies used in this study.
Figure S9 from Hypoxia-Induced Long Noncoding RNA HIF1A-AS2 Regulates Stability of MHC Class I Protein in Head and Neck Cancer
Authors: Liao Tsai-Tsen , Chen Yu-Hsien , Li Zih-Yu , Hsiao An-Ching , Huang Ya-Li , Hao Ruo-Xin , Tai Shyh-Kuan , Chu Pen-Yuan , Shih Jing-Wen , Kung Hsing-Jien , Yang Muh-Hwa
Published: October 2024

Influence of HIF1A-AS2 on normal human gingival epithelial cells.
Supplementary Figure 2 from Intermittent MEK Inhibition with GITR Costimulation Rescues T-cell Function for Increased Efficacy with CTLA-4 Blockade in Solid Tumor Models
Authors: Dong Lauren , Choi Hyejin , Budhu Sadna , Schulze Isabell , Verma Svena , Mangarin Levi M. , Estrada Nevarro Valeria , Mehanna Nezar , Khan Jonathan F. , Venkatesh Divya , Thach Daniel , Rosen Neal , Wolchok Jedd D. , Merghoub Taha
Published: October 2024

Supplementary Figure 2. MEK inhibition with CKI27 increases MHC and checkpoint ligand expression. Murine tumor cell lines were treated with DMSO or CKI27 for 72 hr and either with or without IFNγ (5ng/mL) for the last 24hr; n=3. FACS analysis of representative histograms for the MFI of MHC-I (H2Kb/Kd and H2Db/Dd), MHC-II, PD-L1, CD80 and CD86 are shown.
Supplementary Figure 15 from Intermittent MEK Inhibition with GITR Costimulation Rescues T-cell Function for Increased Efficacy with CTLA-4 Blockade in Solid Tumor Models
Authors: Dong Lauren , Choi Hyejin , Budhu Sadna , Schulze Isabell , Verma Svena , Mangarin Levi M. , Estrada Nevarro Valeria , Mehanna Nezar , Khan Jonathan F. , Venkatesh Divya , Thach Daniel , Rosen Neal , Wolchok Jedd D. , Merghoub Taha
Published: October 2024

Supplementary Figure 15. The triple combination favorably alters the genetic profile of immune cells in the TDLN. LLC tumor bearing mice were treated with vehicle, CKI27, isotypes, GITR, and/or CTLA-4. TLDNs were harvested on day 21 (7 days post treatment). Live CD45+ cells were FACS sorted and processed for sc-RNA sequencing. (A-B) Heatmap showing top genes expressed by each cluster for (A) CD8+ and (B) CD4+ T cells. (C) UMAPs of each treatment groups showing different clusters and annotations. (D) UMAPs of CD8+ and CD4+ T cells from each treatment group showing specific activation genes and proteins.
Figure S4 from Hypoxia-Induced Long Noncoding RNA HIF1A-AS2 Regulates Stability of MHC Class I Protein in Head and Neck Cancer
Authors: Liao Tsai-Tsen , Chen Yu-Hsien , Li Zih-Yu , Hsiao An-Ching , Huang Ya-Li , Hao Ruo-Xin , Tai Shyh-Kuan , Chu Pen-Yuan , Shih Jing-Wen , Kung Hsing-Jien , Yang Muh-Hwa
Published: October 2024

The impact of ectopic HIF1A-AS2 on the expression of HLA-ABC in different human cancer cell lines.
Supplementary Figure 12 from Intermittent MEK Inhibition with GITR Costimulation Rescues T-cell Function for Increased Efficacy with CTLA-4 Blockade in Solid Tumor Models
Authors: Dong Lauren , Choi Hyejin , Budhu Sadna , Schulze Isabell , Verma Svena , Mangarin Levi M. , Estrada Nevarro Valeria , Mehanna Nezar , Khan Jonathan F. , Venkatesh Divya , Thach Daniel , Rosen Neal , Wolchok Jedd D. , Merghoub Taha
Published: October 2024

Supplementary Figure 12. The triple combination increases activation of CD8+ T cells, CD4+ Teffs, and Tregs in CT26 TDLN. (A) Schema of CT26 tumor bearing mice treated with vehicle, CKI27, isotypes, GITR, and/or CTLA-4. All timepoints were harvested on day 21 (7 days post treatment). (B) Absolute number of immune cell populations in the TDLN; n=4-5. (C) Phenotypes of T cells from the TDLN; n=4-5. Data are shown as mean±SEM. One-way ANOVA test with Bonferroni’s correction for multiple comparisons was used in all panels. Significance levels are indicated by asterisks (*p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001).
Figure 7 from Hypoxia-Induced Long Noncoding RNA HIF1A-AS2 Regulates Stability of MHC Class I Protein in Head and Neck Cancer
Authors: Liao Tsai-Tsen , Chen Yu-Hsien , Li Zih-Yu , Hsiao An-Ching , Huang Ya-Li , Hao Ruo-Xin , Tai Shyh-Kuan , Chu Pen-Yuan , Shih Jing-Wen , Kung Hsing-Jien , Yang Muh-Hwa
Published: October 2024

Schematic representation of the study.
Figure 3 from Hypoxia-Induced Long Noncoding RNA HIF1A-AS2 Regulates Stability of MHC Class I Protein in Head and Neck Cancer
Authors: Liao Tsai-Tsen , Chen Yu-Hsien , Li Zih-Yu , Hsiao An-Ching , Huang Ya-Li , Hao Ruo-Xin , Tai Shyh-Kuan , Chu Pen-Yuan , Shih Jing-Wen , Kung Hsing-Jien , Yang Muh-Hwa
Published: October 2024

Impact of HIF1A-AS2 on the expression of MHC-Ⅰ in HNSCC. A, CIBERSORT analysis to compare the proportion of infiltrated immune cells in patients from the TCGA-HNSCC database with high HIF1A-AS2 [HIF1A-AS2(H)] versus low HIF1A-AS2 [HIF1A-AS2(L)]. The infiltrated immune cells that significantly decreased in patients with HIF1A-AS2(H) were labeled in green text and conversely were highlighted in red text. B, CIBERSORT analysis to compare the proportion of CD8+ T cells in the 4 patient subgroups based on high or low HIF1A and high or low HIF1A-AS2: HIF1A-AS2(H)/HIF1A(H), HIF1A-AS2(H)/HIF1A(L), HIF1A-AS2(L)/HIF1A(H), and HIF1A-AS2(L)/HIF1A(L). C, Top: western blots showing the expression of HIF1α and HLA-ABC in SAS (left) and HSC3 (right) cells treated with CoCl2 treated versus corresponding control (Ctrl) and overexpressing HIF1A-AS2 versus control (Vec). Bottom: RT-qPCR for showing the HIF1A-AS expression in the above groups of cells. Data represent the mean ± S.D. n = 3 independent experiments (each experiment contained two technical replicates). D, Top: Representative flow cytometry overlay histograms showing the cell surface expression of HLA-ABC in SAS and HSC3 cells overexpressing HIF1A-AS2 and control cells. Bottom: mean fluorescent intensity quantification was performed for independent replicate experiments (n = 3). E, Top: western blots of the expression of HLA-ABC in SAS HIF1A-AS2 knockdown cells (SAS-sh#1 and SAS-sh#2) under hypoxia-mimic versus normoxia condition. Lower: RT-qPCR for examination of HIF1A-AS2 level in SAS-sh#1 and SAS-sh#2 cells under hypoxia-mimic versus normoxia condition. #1 and #2 represent two different shRNAs. Data represent the mean ± SD. n = 3 independent experiments (each experiment contained two technical replicates). F, Western blots for showing the expression of HLA-ABC in SAS HIF1A-AS2 knockdown cells (SAS-sh#1) and transiently reconstituted with HIF1A-AS2 versus control under hypoxia-mimic conditions. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Figure 2 from Hypoxia-Induced Long Noncoding RNA HIF1A-AS2 Regulates Stability of MHC Class I Protein in Head and Neck Cancer
Authors: Liao Tsai-Tsen , Chen Yu-Hsien , Li Zih-Yu , Hsiao An-Ching , Huang Ya-Li , Hao Ruo-Xin , Tai Shyh-Kuan , Chu Pen-Yuan , Shih Jing-Wen , Kung Hsing-Jien , Yang Muh-Hwa
Published: October 2024

Direct regulation of HIF1A-AS2 by HIF1α. A, ChIP-seq analysis of the HIF1α binding on the regulatory region of HIF1A-AS2 in human umbilical vein cell line (EA.hy926), human prostatic adenocarcinoma cell (PC3), human renal cell carcinoma cell line (RCC4), and human squamous cell carcinoma of the hypopharynx (FaDu). ChIP-seq data were extracted from GEO: GSM3402530, GSM3145502, GSM3417826, and GSM5224574 and analyzed using ChIP-Atlas. B, Top: Schematic representation of the organization of the regulatory region of human HIF1A-AS2 and the luciferase reporter constructs used in the experiment. The HREs are indicated. Bottom: Luciferase reporter assay. Bottom left, 293T cells were co-transfected with HIF1α(ΔODD) /control vector and the reporter plasmid. Lower right, 293T cells were co-transfected with HIF1α(ΔODD) and the indicated reporter plasmid. Data represent the mean ± SD. n = 3 independent experiments (each experiment contains two technical replicates). C, Left top: Western blots of HA for indicating the establishment of the HA-HIF1α(ΔODD) constitutive expression in SAS [HIF1α(ΔODD) versus SAS-vector control (Vec)] cells. Left bottom: RT-qPCR for analyzing the expression of HIF1A-AS2 in SAS-HIF1α(ΔODD) versus SAS-vector control (Vec) cells. Data represent the mean ± S.D. n = 3 independent experiments (each experiment contained two technical replicates). Right top: schema showing the regulatory regions of HIF1A-AS2 and the ChIP/control primers for the experiment. Right bottom: quantitative ChIP for analyzing the enrichment of HIF1α at the HIF1A-AS2 regulatory region in SAS-HIF1α(ΔODD) versus SAS-vector control (Vec) cells. One representative experiment of three independent experiments is shown. The replicates are presented in Supplementary Fig. S2. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Figure 1 from Hypoxia-Induced Long Noncoding RNA HIF1A-AS2 Regulates Stability of MHC Class I Protein in Head and Neck Cancer
Authors: Liao Tsai-Tsen , Chen Yu-Hsien , Li Zih-Yu , Hsiao An-Ching , Huang Ya-Li , Hao Ruo-Xin , Tai Shyh-Kuan , Chu Pen-Yuan , Shih Jing-Wen , Kung Hsing-Jien , Yang Muh-Hwa
Published: October 2024

Hypoxia-induced HIF1A-AS2 enrichment in HNSCC cells and HNSCC-TEXs. A, Heatmaps for showing the RT-qPCR results of the hypoxia relative lncRNA expression in the cellular (left) and exosomal (right) contents of SAS cells. For establishing the hypoxia-mimic environment, SAS cells were treated with CoCl2 versus control for 24 hours. Data represent the mean ± SD. n = 3 independent experiments (each experiment contains two technical replicates). B, RT-qPCR for examining the expression of two candidates of hypoxia-induced lncRNAs in the cellular (left) and exosomal (right) contents of SAS and HSC3 cells. For establishing the hypoxia-mimic environment, SAS and HSC3 cells were treated with CoCl2 versus control for 24 hours. Data represent the mean ± SD. n = 3 independent experiments (each experiment contains two technical replicates). C,HIF1A-AS2 expression in tumor (T, n = 500) versus adjacent normal counterparts (N, n = 44) from TCGA-HNSCC database. D,HIF1A-AS2 expression in tumor (T) versus adjacent normal counterparts (N) of 20 HNSCC paired samples from TVGH (GSE178537). E, Top: Correlation between HIF1A-AS2 and hypoxia signature in the GDC-HNSCC database. Bottom: Correlation between HIF1A-AS2 and hypoxia HIF1A in the GDC-HNSCC database (n = 545). The correlation analysis was performed using the Pearson correlation coefficient. F, The representative confocal image for showing the engulfment of exosomes by SAS cells. The exosomes were derived from hypoxic (Hypo-Exos) or normoxic SAS cells (Nor-Exos). DAPI, 4,6-diamidino-2-phenylindole. Scale bar, 10 μm G, RT-qPCR for examining the HIF1A-AS2 level in SAS cells after treatment with Hypo-Exos versus Nor-Exos. Data represent the mean ± SD. n = 3 independent experiments (each experiment contains two technical replicates). *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Supplementary Figure S3 from MR1 Gene and Protein Expression Are Enhanced by Inhibition of the Extracellular Signal-Regulated Kinase ERK
Authors: Constantin Daniel , Nosi Vladimir , Kehrer Natalie , Vacchini Alessandro , Chancellor Andrew , Contassot Emmanuel , Beshirova Aisha , Prota Gennaro , Navarini Alexander , Mori Lucia , De Libero Gennaro
Published: October 2024

Supplementary Figure S3
Supplementary Figure S2 from The E3 Ubiquitin Ligase FBXO38 Maintains the Antitumor Function of Natural Killer Cells by Sustaining IL15R Signaling
Authors: Shi Yongjing , Zheng Xiaodong , Peng Hui , Xu Chenqi , Sun Rui , Tian Zhigang , Sun Haoyu , Wang Xianwei
Published: October 2024

Supplementary Figure S2. Tumor grown faster in cKO mice than Ncr1Cre/+ mice
Data from Atypical B Cells Promote Cancer Progression and Poor Response to Bacillus Calmette-Guérin in Non–Muscle Invasive Bladder Cancer
Authors: Yolmo Priyanka , Rahimi Sadaf , Chenard Stephen , Conseil Gwenaëlle , Jenkins Danielle , Sachdeva Kartik , Emon Isaac , Hamilton Jake , Xu Minqi , Rangachari Manu , Michaud Eva , Mansure Jose J. , Kassouf Wassim , Berman David M. , Siemens David R. , Koti Madhuri
Published: October 2024

Abstract
Poor response to Bacillus Calmette-Guérin (BCG) immunotherapy remains a major barrier in the management of patients with non–muscle invasive bladder cancer (NMIBC). Multiple factors are associated with poor outcomes, including biological aging and female sex. More recently, it has emerged that a B‐cell–infiltrated pretreatment immune microenvironment of NMIBC tumors can influence the response to intravesically administered BCG. The mechanisms underlying the roles of B cells in NMIBC are poorly understood. Here, we show that B‐cell–dominant tertiary lymphoid structures (TLSs), a hallmark feature of the chronic mucosal immune response, are abundant and located close to the epithelial compartment in pretreatment tumors from BCG non-responders. Digital spatial proteomic profiling of whole tumor sections from male and female patients with NMIBC who underwent treatment with intravesical BCG, revealed higher expression of immune exhaustion–associated proteins within the tumor-adjacent TLSs in both responders and non-responders. Chronic local inflammation, induced by the N-butyl-N-(4-hydroxybutyl) nitrosamine carcinogen, led to TLS formation with recruitment and differentiation of the immunosuppressive atypical B‐cell (ABC) subset within the bladder microenvironment, predominantly in aging female mice compared to their male counterparts. Depletion of ABCs simultaneous to BCG treatment delayed cancer progression in female mice. Our findings provide evidence indicating a role for ABCs in BCG response and will inform future development of therapies targeting the B‐cell–exhaustion axis.
Supplementary Figure S6 from Combined Oxygen-Enhanced MRI and Perfusion Imaging Detect Hypoxia Modification from Banoxantrone and Atovaquone and Track Their Differential Mechanisms of Action
Authors: O’Connor James P.B. , Tessyman Victoria , Little Ross A. , Babur Muhammad , Forster Duncan , Latif Ayşe , Cheung Susan , Lipowska-Bhalla Grazyna , Higgins Geoff S. , Asselin Marie-Claude , Parker Geoff J.M. , Williams Kaye J.
Published: October 2024

Supplementary Figure S6 shows that banoxantrone induces tumor necrosis.
Supplementary Figure S3 from Combined Oxygen-Enhanced MRI and Perfusion Imaging Detect Hypoxia Modification from Banoxantrone and Atovaquone and Track Their Differential Mechanisms of Action
Authors: O’Connor James P.B. , Tessyman Victoria , Little Ross A. , Babur Muhammad , Forster Duncan , Latif Ayşe , Cheung Susan , Lipowska-Bhalla Grazyna , Higgins Geoff S. , Asselin Marie-Claude , Parker Geoff J.M. , Williams Kaye J.
Published: October 2024

Supplementary Figure S3 shows the MRI analysis steps.
Supplementary Figure S2 from Combined Oxygen-Enhanced MRI and Perfusion Imaging Detect Hypoxia Modification from Banoxantrone and Atovaquone and Track Their Differential Mechanisms of Action
Authors: O’Connor James P.B. , Tessyman Victoria , Little Ross A. , Babur Muhammad , Forster Duncan , Latif Ayşe , Cheung Susan , Lipowska-Bhalla Grazyna , Higgins Geoff S. , Asselin Marie-Claude , Parker Geoff J.M. , Williams Kaye J.
Published: October 2024

Supplementary Figure S2: Confirmation that oxygen increases tumor R1.