bluuebunny/crossref_metadata_2025 huggingface dataset:
Table S1 from T-cell Acute Lymphoblastic Leukemia: A Roadmap to Targeted Therapies
Authors: Cordo' Valentina , van der Zwet Jordy C.G. , Canté-Barrett Kirsten , Pieters Rob , Meijerink Jules P.P.
Published: April 2023

Table S1: relevant clinical trials investigating targeted therapies for T-ALL treatment: List of clinical trials investigating the targeted agents described in this review. The clinical trials listed were chosen based on the following two selection criteria: the targeted drug investigated belongs to one of the categories of agents described in the text (modifiers of apoptosis, inhibitors of transcription regulation, signal transduction, cell cycle or immunotherapies) and the trial includes T-ALL patients. * Source: https://clinicaltrials.gov/ Abbreviations: p= pediatric, ya= young adult, a= adults; ALL= acute lymphoblastic leukemia, LBL= lymphoblastic lymphoma, AML= acute myeloid leukemia, MDS= myelodysplastic syndrome, MM= multiple myeloma, Dx= newly diagnosed, R/R= refractory/relapsed; chemo= chemotherapy; dexa= dexamethasone; WT= wild-type; N/A= not applicable, R= recruiting, A= active, C= completed, T= terminated, NR= not yet recruiting.
Supplementary Tables from PRPS-ST: A Protocol-Agnostic Self-training Method for Gene Expression–Based Classification of Blood Cancers
Authors: Jiang Aixiang , Hilton Laura K. , Tang Jeffrey , Rushton Christopher K. , Grande Bruno M. , Scott David W. , Morin Ryan D.
Published: April 2023

Supplementary Tables
Supplementary Methods from Phase II Trial of Pembrolizumab after High-Dose Cytarabine in Relapsed/Refractory Acute Myeloid Leukemia
Authors: Zeidner Joshua F. , Vincent Benjamin G. , Ivanova Anastasia , Moore Dominic , McKinnon Karen P. , Wilkinson Alec D. , Mukhopadhyay Rupkatha , Mazziotta Francesco , Knaus Hanna A. , Foster Matthew C. , Coombs Catherine C. , Jamieson Katarzyna , Van Deventer Hendrik , Webster Jonathan A. , Prince Gabrielle T. , DeZern Amy E. , Smith B. Douglas , Levis Mark J. , Montgomery Nathan D. , Luznik Leo , Serody Jonathan S. , Gojo Ivana
Published: April 2023

Supplemental Methods
Supplementary Tables from Dissecting Clonal Hematopoiesis in Tissues of Patients with Classic Hodgkin Lymphoma
Authors: Venanzi Alessandra , Marra Andrea , Schiavoni Gianluca , Milner Sara G. , Limongello Roberto , Santi Alessia , Pettirossi Valentina , Ultimo Simona , Tasselli Luisa , Pucciarini Alessandra , Falini Lorenza , Sciabolacci Sofia , Martelli Maria Paola , Sportoletti Paolo , Ascani Stefano , Falini Brunangelo , Tiacci Enrico
Published: April 2023

Supplementary Tables show: i) Supplementary Table 1. Genes subjected to targeted deep sequencing; ii) Supplementary Table 2. CHIP-associated mutations observed by NGS in the cohort of 39 cHL patients; iii)Supplementary Table 3. List of somatic mutations observed in the samples of Case-1 by targeted NGS.
Supplementary Figures from Dissecting Clonal Hematopoiesis in Tissues of Patients with Classic Hodgkin Lymphoma
Authors: Venanzi Alessandra , Marra Andrea , Schiavoni Gianluca , Milner Sara G. , Limongello Roberto , Santi Alessia , Pettirossi Valentina , Ultimo Simona , Tasselli Luisa , Pucciarini Alessandra , Falini Lorenza , Sciabolacci Sofia , Martelli Maria Paola , Sportoletti Paolo , Ascani Stefano , Falini Brunangelo , Tiacci Enrico
Published: April 2023

Supplementary Figures show: i) Fig. S1: Microdissection of HRS cells and reactive lymphocytes from the cHL tissue; ii) Fig. S2: Tissue involvement by clonal hematopoiesis (in cHL Case 2; iii) Fig.S3: T-cell receptor gamma gene rearrangement analysis in cHL tissues with extensive clonal hematopoiesis (CH).
Supplementary Figure 1-9 from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation
Authors: Gulla Annamaria , Morelli Eugenio , Samur Mehmet K. , Botta Cirino , Hideshima Teru , Bianchi Giada , Fulciniti Mariateresa , Malvestiti Stefano , Prabhala Rao H. , Talluri Srikanth , Wen Kenneth , Tai Yu-Tzu , Richardson Paul G. , Chauhan Dharminder , Sewastianik Tomasz , Carrasco Ruben D. , Munshi Nikhil C. , Anderson Kenneth C.
Published: April 2023

Supp. Fig. 1 shows that bortezomib induces ICD in vitro. Suppl. Fig.2 shows that bortezomib treatment of co-culture of dendritic and T cells does not induce T cell maturation. Suppl. Fig. 3 shows that bortezomib-induced MM cell death promotes proliferation of CD4+ and CD8+ naïve T cells. Suppl. Fig.4 shows that bortezomib treatment generates a robust immune response against MM cells. Suppl. Fig. 5 shows pathways enriched by bortezomib treatment in vivo. Suppl. Fig. 6 shows Gene Ontology analysis of ICD signature genes. Suppl. Fig. 7 shows that MM cells engage in a type-I IFN response after treatment with bortezomib. Suppl. Fig. 8 shows type-I IFN response after bortezomib in MM is STING dependent. Suppl. Fig. 9 shows STING agonists potentiate bortezomib-induced anti-tumor immunity.
Supplementary Data from Next-Generation Sequencing of Minimal Residual Disease for Predicting Relapse after Tisagenlecleucel in Children and Young Adults with Acute Lymphoblastic Leukemia
Authors: Pulsipher Michael A. , Han Xia , Maude Shannon L. , Laetsch Theodore W. , Qayed Muna , Rives Susana , Boyer Michael W. , Hiramatsu Hidefumi , Yanik Gregory A. , Driscoll Tim , Myers G. Doug , Bader Peter , Baruchel Andre , Buechner Jochen , Stefanski Heather E. , Kalfoglou Creton , Nguyen Kevin , Waldron Edward R. , Thudium Mueller Karen , Maier Harald J. , Kari Gabor , Grupp Stephan A.
Published: April 2023

Supplementary Data from Next-Generation Sequencing of Minimal Residual Disease for Predicting Relapse after Tisagenlecleucel in Children and Young Adults with Acute Lymphoblastic Leukemia
Supplementary Figure from Anti-spike T-cell and Antibody Responses to SARS-CoV-2 mRNA Vaccines in Patients with Hematologic Malignancies
Authors: Greenberger Lee M. , Saltzman Larry A. , Gruenbaum Lore M. , Xu Jun , Reddy Sneha T. , Senefeld Jonathon W. , Johnson Patrick W. , Fields Paul A. , Sanders Catherine , DeGennaro Louis J. , Nichols Gwen L.
Published: April 2023

Supplementary Figure from Anti-spike T-cell and Antibody Responses to SARS-CoV-2 mRNA Vaccines in Patients with Hematologic Malignancies
Supplementary Figure from Progenitor Hierarchy of Chronic Myelomonocytic Leukemia Identifies Inflammatory Monocytic-Biased Trajectory Linked to Worse Outcomes
Authors: Ferrall-Fairbanks Meghan C. , Dhawan Abhishek , Johnson Brian , Newman Hannah , Volpe Virginia , Letson Christopher , Ball Markus , Hunter Anthony M. , Balasis Maria E. , Kruer Traci , Ben-Crentsil Nana Adjoa , Kroeger Jodi L. , Balderas Robert , Komrokji Rami S. , Sallman David A. , Zhang Jing , Bejar Rafael , Altrock Philipp M. , Padron Eric
Published: April 2023

Supplementary Figure from Progenitor Hierarchy of Chronic Myelomonocytic Leukemia Identifies Inflammatory Monocytic-Biased Trajectory Linked to Worse Outcomes
Supplementary Figures from A Therapeutically Targetable NOTCH1–SIRT1–KAT7 Axis in T-cell Leukemia
Authors: Lancho Olga , Singh Amartya , da Silva-Diz Victoria , Aleksandrova Maya , Khatun Jesminara , Tottone Luca , Nunes Patricia Renck , Luo Shirley , Zhao Caifeng , Zheng Haiyan , Chiles Eric , Zuo Zhenyu , Rocha Pedro P. , Su Xiaoyang , Khiabanian Hossein , Herranz Daniel
Published: April 2023

Supplementary Figures S1-S7 and Legends
Data from Targeting MEF2D-fusion Oncogenic Transcriptional Circuitries in B-cell Precursor Acute Lymphoblastic Leukemia
Authors: Tsuzuki Shinobu , Yasuda Takahiko , Kojima Shinya , Kawazu Masahito , Akahane Koshi , Inukai Takeshi , Imaizumi Masue , Morishita Takanobu , Miyamura Koichi , Ueno Toshihide , Karnan Sivasundaram , Ota Akinobu , Hyodo Toshinori , Konishi Hiroyuki , Sanada Masashi , Nagai Hirokazu , Horibe Keizo , Tomita Akihiro , Suzuki Kyogo , Muramatsu Hideki , Takahashi Yoshiyuki , Miyazaki Yasushi , Matsumura Itaru , Kiyoi Hitoshi , Hosokawa Yoshitaka , Mano Hiroyuki , Hayakawa Fumihiko
Published: April 2023

Abstract
The cellular context that integrates gene expression, signaling, and metabolism dictates the oncogenic behavior and shapes the treatment responses in distinct cancer types. Although chimeric fusion proteins involving transcription factors (TF) are hallmarks of many types of acute lymphoblastic leukemia (ALL), therapeutically targeting the fusion proteins is a challenge. In this work, we characterize the core regulatory circuitry (CRC; interconnected autoregulatory loops of TFs) of B-ALL involving MEF2D-fusions and identify MEF2D-fusion and SREBF1 TFs as crucial CRC components. By gene silencing and pharmacologic perturbation, we reveal that the CRC integrates the pre-B-cell receptor (BCR) and lipid metabolism to maintain itself and govern malignant phenotypes. Small-molecule inhibitors of pre-BCR signaling and lipid biosynthesis disrupt the CRC and silence the MEF2D fusion in cell culture and show therapeutic efficacy in xenografted mice. Therefore, pharmacologic disruption of CRC presents a potential therapeutic strategy to target fusion protein–driven leukemia.
Significance:
Cancer type–specific gene expression is governed by transcription factors involved in a highly interconnected autoregulatory loop called CRC. Here, we characterized fusion protein–driven CRC and identified its pharmacologic vulnerabilities, opening therapeutic avenues to indirectly target fusion-driven leukemia by disrupting its CRC.

See related commentary by Sadras and Müschen, p. 18.

This article is highlighted in the In This Issue feature, p. 5
Data from An Autochthonous Mouse Model of Myd88- and BCL2-Driven Diffuse Large B-cell Lymphoma Reveals Actionable Molecular Vulnerabilities
Authors: Flümann Ruth , Rehkämper Tim , Nieper Pascal , Pfeiffer Pauline , Holzem Alessandra , Klein Sebastian , Bhatia Sanil , Kochanek Moritz , Kisis Ilmars , Pelzer Benedikt W. , Ahlert Heinz , Hauer Julia , da Palma Guerreiro Alexandra , Ryan Jeremy A. , Reimann Maurice , Riabinska Arina , Wiederstein Janica , Krüger Marcus , Deckert Martina , Altmüller Janine , Klatt Andreas R. , Frenzel Lukas P. , Pasqualucci Laura , Béguelin Wendy , Melnick Ari M. , Sander Sandrine , Montesinos-Rongen Manuel , Brunn Anna , Lohneis Philipp , Büttner Reinhard , Kashkar Hamid , Borkhardt Arndt , Letai Anthony , Persigehl Thorsten , Peifer Martin , Schmitt Clemens A. , Reinhardt Hans Christian , Knittel Gero
Published: April 2023

Abstract
Based on gene expression profiles, diffuse large B-cell lymphoma (DLBCL) is subdivided into germinal center B-cell–like (GCB) and activated B-cell–like (ABC) DLBCL. Two of the most common genomic aberrations in ABC-DLBCL are mutations in MYD88 as well as BCL2 copy-number gains. Here, we employ immune phenotyping, RNA sequencing, and whole-exome sequencing to characterize a Myd88- and BCL2-driven mouse model of ABC-DLBCL. We show that this model resembles features of human ABC-DLBCL. We further demonstrate an actionable dependence of our murine ABC-DLBCL model on BCL2. This BCL2 dependence was also detectable in human ABC-DLBCL cell lines. Moreover, human ABC-DLBCLs displayed increased PD-L1 expression compared with GCB-DLBCL. In vivo experiments in our ABC-DLBCL model showed that combined venetoclax and PD-1 blockade significantly increased the overall survival of lymphoma-bearing animals, indicating that this combination may be a viable option for selected human ABC-DLBCL cases harboring MYD88 and BCL2 aberrations.
Significance:
Oncogenic Myd88 and BCL2 cooperate in murine DLBCL lymphomagenesis. The resulting lymphomas display morphologic and transcriptomic features reminiscent of human ABC-DLBCL. Data derived from our Myd88/BCL2-driven autochthonous model demonstrate that combined BCL2 and PD-1 blockade displays substantial preclinical antilymphoma activity, providing preclinical proof-of-concept data, which pave the way for clinical translation.

This article is highlighted in the In This Issue feature, p. 1
Data from Clinical Significance of Novel Subtypes of Acute Lymphoblastic Leukemia in the Context of Minimal Residual Disease–Directed Therapy
Authors: Jeha Sima , Choi John , Roberts Kathryn G. , Pei Deqing , Coustan-Smith Elaine , Inaba Hiroto , Rubnitz Jeffrey E. , Ribeiro Raul C. , Gruber Tanja A. , Raimondi Susana C. , Karol Seth E. , Qu Chunxu , Brady Samuel W. , Gu Zhaohui , Yang Jun J. , Cheng Cheng , Downing James R. , Evans Williams E. , Relling Mary V. , Campana Dario , Mullighan Charles G. , Pui Ching-Hon
Published: April 2023

Abstract
We evaluated clinical significance of recently identified subtypes of acute lymphoblastic leukemia (ALL) in 598 children treated with minimal residual disease (MRD)–directed therapy. Among the 16 B-cell ALL (B-ALL) and 8 T-cell ALL subtypes identified by next-generation sequencing, ETV6–RUNX1, high-hyperdiploid, and DUX4-rearranged B-ALL had the best 5-year event-free survival rates (95.0%–98.4%); TCF3–PBX1, PAX5-altered (PAX5alt), T-cell, early T-cell precursor (ETP), intrachromosomal amplification of chromosome 21 (iAMP21), and hypodiploid ALL intermediate rates (80.0%–88.2%); and BCR–ABL1, BCR–ABL1-like, ETV6–RUNX1-like, and KMT2A-rearranged ALL the worst rates (64.1%–76.2%). All but 3 of the 142 patients with day 8 blood MRD <0.01% remained in remission. Among new subtypes, intensified therapy based on day 15 MRD ≥1% improved outcome of DUX4-rearranged, BCR–ABL1-like, and ZNF384-rearranged ALL, and achievement of day 42 MRD <0.01% did not preclude relapse of PAX5alt, MEF2D-rearranged, and ETV6–RUNX1-like ALL. Thus, new subtypes including DUX4-rearranged, PAX5alt, BCR–ABL1-like, ETV6–RUNX1-like, MEF2D-rearranged, and ZNF384-rearranged ALL have important prognostic and therapeutic implications.
Significance:
Genomic analyses and MRD should be used together for risk-directed treatment of childhood ALL. Six recently described subtypes—DUX4-rearranged, PAX5alt, BCR–ABL1-like, ETV6–RUNX1-like, MEF2D-rearranged, and ZNF384-rearranged ALL—had prognostic and therapeutic significance with contemporary risk-directed treatment.

See related commentary by Segers and Cools, p. 294.

See related video from the AACR Annual Meeting 2021: https://vimeo.com/558556916
Data from ZBTB33 Is Mutated in Clonal Hematopoiesis and Myelodysplastic Syndromes and Impacts RNA Splicing
Authors: Beauchamp Ellen M. , Leventhal Matthew , Bernard Elsa , Hoppe Emma R. , Todisco Gabriele , Creignou Maria , Gallì Anna , Castellano Cecilia A. , McConkey Marie , Tarun Akansha , Wong Waihay , Schenone Monica , Stanclift Caroline , Tanenbaum Benjamin , Malolepsza Edyta , Nilsson Björn , Bick Alexander G. , Weinstock Joshua S. , Miller Mendy , Niroula Abhishek , Dunford Andrew , Taylor-Weiner Amaro , Wood Timothy , Barbera Alex , Anand Shankara , Psaty Bruce M. , Desai Pinkal , Cho Michael H. , Johnson Andrew D. , Loos Ruth , MacArthur Daniel G. , Lek Monkol , Neuberg Donna S. , Lage Kasper , Carr Steven A. , Hellstrom-Lindberg Eva , Malcovati Luca , Papaemmanuil Elli , Stewart Chip , Getz Gad , Bradley Robert K. , Jaiswal Siddhartha , Ebert Benjamin L.
Published: April 2023

Abstract
Clonal hematopoiesis results from somatic mutations in cancer driver genes in hematopoietic stem cells. We sought to identify novel drivers of clonal expansion using an unbiased analysis of sequencing data from 84,683 persons and identified common mutations in the 5-methylcytosine reader ZBTB33 as well as in YLPM1, SRCAP, and ZNF318. We also identified these mutations at low frequency in patients with myelodysplastic syndrome. Zbtb33-edited mouse hematopoietic stem and progenitor cells exhibited a competitive advantage in vivo and increased genome-wide intron retention. ZBTB33 mutations potentially link DNA methylation and RNA splicing, the two most commonly mutated pathways in clonal hematopoiesis and myelodysplastic syndromes.
Significance:
Mutations in known driver genes can be found in only about half of individuals with clonal hematopoiesis. Here, we performed a somatic mutation discovery effort in nonmalignant blood samples, which identified novel candidate genes that may play biological roles in hematopoietic stem cell expansion and hematologic malignancies.

This article is highlighted in the In This Issue feature, p. 403
Data from Predictors of Humoral Response to SARS-CoV-2 Vaccination after Hematopoietic Cell Transplantation and CAR T-cell Therapy
Authors: Tamari Roni , Politikos Ioannis , Knorr David A. , Vardhana Santosha A. , Young Jennifer C. , Marcello LeeAnn T. , Doddi Sital , Devlin Sean M. , Ramanathan Lakshmi V. , Pessin Melissa S. , Dunn Erica , Palazzo Meighan , Bravo Christina D. , Papanicolaou Genovefa A. , Kamboj Mini , Perales Miguel Angel , Chung David J. , Shah Gunjan L.
Published: April 2023

Abstract
Cellular therapies including allogeneic hematopoietic cell transplant (allo-HCT) and autologous hematopoietic cell transplant (auto-HCT) and chimeric antigen receptor (CAR) T-cell therapy render patients severely immunocompromised for extended periods after therapy, and data on responses to COVID-19 vaccines are limited. We analyzed anti–SARS-CoV-2 spike IgG Ab (spike Ab) titers and neutralizing Ab among 217 recipients of cellular treatments (allo-HCT, n = 149; auto-HCT, n = 61; CAR T-cell therapy, n = 7). At 3 months after vaccination, 188 patients (87%) had positive spike Ab levels and 139 (77%) had positive neutralization activity compared with 100% for both in 54 concurrent healthy controls. Time from cellular therapy to vaccination and immune recovery post–cellular therapy were associated with response. Vaccination against COVID-19 is an important component of post–cellular therapy care, and predictors of quantitative and qualitative response are critical in informing clinical decisions about optimal timing of vaccines and the requirement for booster doses.
Significance:
Identifying predictors of response to vaccination against SARS-CoV-2 in patients following cellular therapy is critical to managing this highly vulnerable patient population. To date, this is the most comprehensive study evaluating quantitative and qualitative responses to vaccination, providing parameters most predictive of response and potentially informing booster vaccination strategies.

See related article by Chung et al., p. 568.

This article is highlighted in the In This Issue feature, p. 549
Data from Aberrant Extrafollicular B Cells, Immune Dysfunction, Myeloid Inflammation, and MyD88-Mutant Progenitors Precede Waldenstrom Macroglobulinemia
Authors: Kaushal Akhilesh , Nooka Ajay K. , Carr Allison R. , Pendleton Katherine E. , Barwick Benjamin G. , Manalo Julia , McCachren Samuel S. , Gupta Vikas A. , Joseph Nisha S. , Hofmeister Craig C. , Kaufman Jonathan L. , Heffner Leonard T. , Ansell Stephen M. , Boise Lawrence H. , Lonial Sagar , Dhodapkar Kavita M. , Dhodapkar Madhav V.
Published: April 2023

Abstract
Waldenstrom macroglobulinemia (WM) and its precursor IgM gammopathy are distinct disorders characterized by clonal mature IgM-expressing B-cell outgrowth in the bone marrow. Here, we show by high-dimensional single-cell immunogenomic profiling of patient samples that these disorders originate in the setting of global B-cell compartment alterations, characterized by expansion of genomically aberrant extrafollicular B cells of the nonmalignant clonotype. Alterations in the immune microenvironment preceding malignant clonal expansion include myeloid inflammation and naïve B- and T-cell depletion. Host response to these early lesions involves clone-specific T-cell immunity that may include MYD88 mutation–specific responses. Hematopoietic progenitors carry the oncogenic MYD88 mutations characteristic of the malignant WM clone. These data support a model for WM pathogenesis wherein oncogenic alterations and signaling in progenitors, myeloid inflammation, and global alterations in extrafollicular B cells create the milieu promoting extranodal pattern of growth in differentiated malignant cells.
Significance:
These data provide evidence that growth of the malignant clone in WM is preceded by expansion of extrafollicular B cells, myeloid inflammation, and immune dysfunction in the preneoplastic phase. These changes may be related in part to MYD88 oncogenic signaling in pre–B progenitor cells and suggest a novel model for WM pathogenesis.

This article is highlighted in the In This Issue feature, p. 549
Data from Integrated Genomic Analysis Identifies UBTF Tandem Duplications as a Recurrent Lesion in Pediatric Acute Myeloid Leukemia
Authors: Umeda Masayuki , Ma Jing , Huang Benjamin J. , Hagiwara Kohei , Westover Tamara , Abdelhamed Sherif , Barajas Juan M. , Thomas Melvin E. , Walsh Michael P. , Song Guangchun , Tian Liqing , Liu Yanling , Chen Xiaolong , Kolekar Pandurang , Tran Quang , Foy Scott G. , Maciaszek Jamie L. , Kleist Andrew B. , Leonti Amanda R. , Ju Bengsheng , Easton John , Wu Huiyun , Valentine Virginia , Valentine Marcus B. , Liu Yen-Chun , Ries Rhonda E. , Smith Jenny L. , Parganas Evan , Iacobucci Ilaria , Hiltenbrand Ryan , Miller Jonathan , Myers Jason R. , Rampersaud Evadnie , Rahbarinia Delaram , Rusch Michael , Wu Gang , Inaba Hiroto , Wang Yi-Cheng , Alonzo Todd A. , Downing James R. , Mullighan Charles G. , Pounds Stanley , Babu M. Madan , Zhang Jinghui , Rubnitz Jeffrey E. , Meshinchi Soheil , Ma Xiaotu , Klco Jeffery M.
Published: April 2023

Abstract
The genetics of relapsed pediatric acute myeloid leukemia (AML) has yet to be comprehensively defined. Here, we present the spectrum of genomic alterations in 136 relapsed pediatric AMLs. We identified recurrent exon 13 tandem duplications (TD) in upstream binding transcription factor (UBTF) in 9% of relapsed AML cases. UBTF-TD AMLs commonly have normal karyotype or trisomy 8 with cooccurring WT1 mutations or FLT3-ITD but not other known oncogenic fusions. These UBTF-TD events are stable during disease progression and are present in the founding clone. In addition, we observed that UBTF-TD AMLs account for approximately 4% of all de novo pediatric AMLs, are less common in adults, and are associated with poor outcomes and MRD positivity. Expression of UBTF-TD in primary hematopoietic cells is sufficient to enhance serial clonogenic activity and to drive a similar transcriptional program to UBTF-TD AMLs. Collectively, these clinical, genomic, and functional data establish UBTF-TD as a new recurrent mutation in AML.
Significance:
We defined the spectrum of mutations in relapsed pediatric AML and identified UBTF-TDs as a new recurrent genetic alteration. These duplications are more common in children and define a group of AMLs with intermediate-risk cytogenetic abnormalities, FLT3-ITD and WT1 alterations, and are associated with poor outcomes.

See related commentary by Hasserjian and Nardi, p. 173.

This article is highlighted in the In This Issue feature, p. 171.
Data from Modulation of CD22 Protein Expression in Childhood Leukemia by Pervasive Splicing Aberrations: Implications for CD22-Directed Immunotherapies
Authors: Zheng Sisi , Gillespie Elisabeth , Naqvi Ammar S. , Hayer Katharina E. , Ang Zhiwei , Torres-Diz Manuel , Quesnel-Vallières Mathieu , Hottman David A. , Bagashev Asen , Chukinas John , Schmidt Carolin , Asnani Mukta , Shraim Rawan , Taylor Deanne M. , Rheingold Susan R. , O'Brien Maureen M. , Singh Nathan , Lynch Kristen W. , Ruella Marco , Barash Yoseph , Tasian Sarah K. , Thomas-Tikhonenko Andrei
Published: April 2023

Abstract
Downregulation of surface epitopes causes postimmunotherapy relapses in B-lymphoblastic leukemia (B-ALL). Here we demonstrate that mRNA encoding CD22 undergoes aberrant splicing in B-ALL. We describe the plasma membrane–bound CD22 Δex5–6 splice isoform, which is resistant to chimeric antigen receptor (CAR) T cells targeting the third immunoglobulin-like domain of CD22. We also describe splice variants skipping the AUG-containing exon 2 and failing to produce any identifiable protein, thereby defining an event that is rate limiting for epitope presentation. Indeed, forcing exon 2 skipping with morpholino oligonucleotides reduced CD22 protein expression and conferred resistance to the CD22-directed antibody–drug conjugate inotuzumab ozogamicin in vitro. Furthermore, among inotuzumab-treated pediatric patients with B-ALL, we identified one nonresponder in whose leukemic blasts Δex2 isoforms comprised the majority of CD22 transcripts. In a second patient, a sharp reduction in CD22 protein levels during relapse was driven entirely by increased CD22 exon 2 skipping. Thus, dysregulated CD22 splicing is a major mechanism of epitope downregulation and ensuing resistance to immunotherapy.
Significance:
The mechanism(s) underlying downregulation of surface CD22 following CD22-directed immunotherapy remains underexplored. Our biochemical and correlative studies demonstrate that in B-ALL, CD22 expression levels are controlled by inclusion/skipping of CD22 exon 2. Thus, aberrant splicing of CD22 is an important driver/biomarker of de novo and acquired resistance to CD22-directed immunotherapies.

See the interview with Sarah K. Tasian, MD, and Andrei Thomas-Tikhonenko, PhD, corecipients of the 2024 Blood Cancer Discovery Award for Outstanding Journal Article: https://vimeo.com/992990779

See related commentary by Bourcier and Abdel-Wahab, p. 87.

This article is highlighted in the In This Issue feature, p. 85.
Data from Txnip Enhances Fitness of Dnmt3a-Mutant Hematopoietic Stem Cells via p21
Authors: Zhang Christine R. , Ostrander Elizabeth L. , Kukhar Ostap , Mallaney Cates , Sun Jiameng , Haussler Emily , Celik Hamza , Koh Won Kyun , King Katherine Y. , Gontarz Paul , Challen Grant A.
Published: April 2023

Abstract
Clonal hematopoiesis (CH) refers to the age-related expansion of specific clones in the blood system, and manifests from somatic mutations acquired in hematopoietic stem cells (HSCs). Most CH variants occur in the gene DNMT3A, but while DNMT3A-mutant CH becomes almost ubiquitous in aging humans, a unifying molecular mechanism to illuminate how DNMT3A-mutant HSCs outcompete their counterparts is lacking. Here, we used interferon gamma (IFNγ) as a model to study the mechanisms by which Dnmt3a mutations increase HSC fitness under hematopoietic stress. We found Dnmt3a-mutant HSCs resist IFNγ-mediated depletion, and IFNγ-signaling is required for clonal expansion of Dnmt3a-mutant HSCs in vivo. Mechanistically, DNA hypomethylation–associated overexpression of Txnip in Dnmt3a-mutant HSCs leads to p53 stabilization and upregulation of p21. This preserves the functional potential of Dnmt3a-mutant HSCs through increased quiescence and resistance to IFNγ-induced apoptosis. These data identify a previously undescribed mechanism to explain increased fitness of DNMT3A-mutant clones under hematopoietic stress.
Significance:
DNMT3A mutations are common variants in clonal hematopoiesis, and recurrent events in blood cancers. Yet the mechanisms by which these mutations provide hematopoietic stem cells a competitive advantage as a precursor to malignant transformation remain unclear. Here, we use inflammatory stress to uncover molecular mechanisms leading to this fitness advantage.

See related commentary by De Dominici and DeGregori, p. 178.

This article is highlighted in the In This Issue feature, p. 171
Data from ZNF384 Fusion Oncoproteins Drive Lineage Aberrancy in Acute Leukemia
Authors: Dickerson Kirsten M. , Qu Chunxu , Gao Qingsong , Iacobucci Ilaria , Gu Zhaohui , Yoshihara Hiroki , Backhaus Emily A. , Chang Yunchao , Janke Laura J. , Xu Beisi , Wu Gang , Papachristou Evangelia K. , D'Santos Clive S. , Roberts Kathryn G. , Mullighan Charles G.
Published: April 2023

Abstract
ZNF384-rearranged fusion oncoproteins (FO) define a subset of lineage ambiguous leukemias, but their mechanistic role in leukemogenesis and lineage ambiguity is poorly understood. Using viral expression in mouse and human hematopoietic stem and progenitor cells (HSPC) and a Ep300::Znf384 knockin mouse model, we show that ZNF384 FO promote hematopoietic expansion, myeloid lineage skewing, and self-renewal. In mouse HSPCs, concomitant lesions, such as NRASG12D, were required for fully penetrant leukemia, whereas in human HSPCs, expression of ZNF384 FO drove B/myeloid leukemia, with sensitivity of a ZNF384-rearranged xenograft to FLT3 inhibition in vivo. Mechanistically, ZNF384 FO occupy a subset of predominantly intragenic/enhancer regions with increased histone 3 lysine acetylation and deregulate expression of hematopoietic stem cell transcription factors. These data define a paradigm for FO-driven lineage ambiguous leukemia, in which expression in HSPCs results in deregulation of lineage-specific genes and hematopoietic skewing, progressing to full leukemia in the context of proliferative stress.
Significance:
Expression of ZNF384 FO early in hematopoiesis results in binding and deregulation of key hematopoietic regulators, skewing of hematopoiesis, and priming for leukemic transformation. These results reveal the interplay between cell of origin and expression of ZNF384 FO to mediate lineage ambiguity and leukemia development.

This article is highlighted in the In This Issue feature, p. 171
Data from Deep Morphology Learning Enhances Ex Vivo Drug Profiling-Based Precision Medicine
Authors: Heinemann Tim , Kornauth Christoph , Severin Yannik , Vladimer Gregory I. , Pemovska Tea , Hadzijusufovic Emir , Agis Hermine , Krauth Maria-Theresa , Sperr Wolfgang R. , Valent Peter , Jäger Ulrich , Simonitsch-Klupp Ingrid , Superti-Furga Giulio , Staber Philipp B. , Snijder Berend
Published: April 2023

Abstract
Drug testing in patient biopsy-derived cells can identify potent treatments for patients suffering from relapsed or refractory hematologic cancers. Here we investigate the use of weakly supervised deep learning on cell morphologies (DML) to complement diagnostic marker-based identification of malignant and nonmalignant cells in drug testing. Across 390 biopsies from 289 patients with diverse blood cancers, DML-based drug responses show improved reproducibility and clustering of drugs with the same mode of action. DML does so by adapting to batch effects and by autonomously recognizing disease-associated cell morphologies. In a post hoc analysis of 66 patients, DML-recommended treatments led to improved progression-free survival compared with marker-based recommendations and physician's choice–based treatments. Treatments recommended by both immunofluorescence and DML doubled the fraction of patients achieving exceptional clinical responses. Thus, DML-enhanced ex vivo drug screening is a promising tool in the identification of effective personalized treatments.
Significance:
We have recently demonstrated that image-based drug screening in patient samples identifies effective treatment options for patients with advanced blood cancers. Here we show that using deep learning to identify malignant and nonmalignant cells by morphology improves such screens. The presented workflow is robust, automatable, and compatible with clinical routine.

This article is highlighted in the In This Issue feature, p. 476
Data from Anti-BCMA/CD19 CAR T Cells with Early Immunomodulatory Maintenance for Multiple Myeloma Responding to Initial or Later-Line Therapy
Authors: Garfall Alfred L. , Cohen Adam D. , Susanibar-Adaniya Sandra P. , Hwang Wei-Ting , Vogl Dan T. , Waxman Adam J. , Lacey Simon F. , Gonzalez Vanessa E. , Fraietta Joseph A. , Gupta Minnal , Kulikovskaya Irina , Tian Lifeng , Chen Fang , Koterba Natalka , Bartoszek Robert L. , Patchin Margaret , Xu Rong , Plesa Gabriela , Siegel Don L. , Brennan Andrea , Nelson Anne Marie , Ferthio Regina , Cosey Angela , Shea Kim-Marie , Leskowitz Rachel , Four Megan , Wilson Wesley V. , Miao Fei , Lancaster Eric , Carreno Beatriz M. , Linette Gerald P. , Hexner Elizabeth O. , Young Regina M. , Bu Dexiu , Mansfield Keith G. , Brogdon Jennifer L. , June Carl H. , Milone Michael C. , Stadtmauer Edward A.
Published: April 2023

Abstract
We conducted a phase I clinical trial of anti-BCMA chimeric antigen receptor T cells (CART-BCMA) with or without anti-CD19 CAR T cells (huCART19) in multiple myeloma (MM) patients responding to third- or later-line therapy (phase A, N = 10) or high-risk patients responding to first-line therapy (phase B, N = 20), followed by early lenalidomide or pomalidomide maintenance. We observed no high-grade cytokine release syndrome (CRS) and only one instance of low-grade neurologic toxicity. Among 15 subjects with measurable disease, 10 exhibited partial response (PR) or better; among 26 subjects responding to prior therapy, 9 improved their response category and 4 converted to minimal residual disease (MRD)–negative complete response/stringent complete response. Early maintenance therapy was safe, feasible, and coincided in some patients with CAR T-cell reexpansion and late-onset, durable clinical response. Outcomes with CART-BCMA + huCART19 were similar to CART-BCMA alone. Collectively, our results demonstrate favorable safety, pharmacokinetics, and antimyeloma activity of dual-target CAR T-cell therapy in early lines of MM treatment.
Significance:
CAR T cells in early lines of MM therapy could be safer and more effective than in the advanced setting, where prior studies have focused. We evaluated the safety, pharmacokinetics, and efficacy of CAR T cells in patients with low disease burden, responding to current therapy, combined with standard maintenance therapy.

This article is highlighted in the In This Issue feature, p. 101
Supplementary Figures S1-S12 from Multiple germline events contribute to cancer development in patients with Li-Fraumeni syndrome
Authors: Subasri Vallijah , Light Nicholas , Kanwar Nisha , Brzezinski Jack , Luo Ping , Hansford Jordan R , Cairney Elizabeth , Portwine Carol , Elser Christine , Finlay Jonathan L. , Nichols Kim E. , Alon Noa , Brunga Ledia , Anson Jo , Kohlmann Wendy , de Andrade Kelvin C. , Khincha Payal P. , Savage Sharon A. , Schiffman Joshua D , Weksberg Rosanna , Pugh Trevor J. , Villani Anita , Shlien Adam , Goldenberg Anna , Malkin David
Published: April 2023

Supplementary Figures
Supplementary Data S3 from Multiple germline events contribute to cancer development in patients with Li-Fraumeni syndrome
Authors: Subasri Vallijah , Light Nicholas , Kanwar Nisha , Brzezinski Jack , Luo Ping , Hansford Jordan R , Cairney Elizabeth , Portwine Carol , Elser Christine , Finlay Jonathan L. , Nichols Kim E. , Alon Noa , Brunga Ledia , Anson Jo , Kohlmann Wendy , de Andrade Kelvin C. , Khincha Payal P. , Savage Sharon A. , Schiffman Joshua D , Weksberg Rosanna , Pugh Trevor J. , Villani Anita , Shlien Adam , Goldenberg Anna , Malkin David
Published: April 2023

1000G Variants
Supplementary Table 2 from Resolving the Heterogeneous Tumor-Centric Cellular Neighborhood through Multiplexed, Spatial Paracrine Interactions in the Setting of Immune Checkpoint Blockade
Authors: Maus Rachel L.G. , Leontovich Alexey A. , Moore Raymond M. , Becher Laura , Nevala Wendy K. , Flotte Thomas J. , Guo Ruifeng , Schimke Jill M. , Dicke Betty A. , Yan Yiyi , Markovic Svetomir N.
Published: April 2023

Summary data of FOV distribution, single cells segmented, classified and clinical response to therapy
Supplementary Figure 1 from Resolving the Heterogeneous Tumor-Centric Cellular Neighborhood through Multiplexed, Spatial Paracrine Interactions in the Setting of Immune Checkpoint Blockade
Authors: Maus Rachel L.G. , Leontovich Alexey A. , Moore Raymond M. , Becher Laura , Nevala Wendy K. , Flotte Thomas J. , Guo Ruifeng , Schimke Jill M. , Dicke Betty A. , Yan Yiyi , Markovic Svetomir N.
Published: April 2023

Phenotypic Cell Classification Tree
Supplementary Materials and Methods, Figures 1-6 from MYCMI-7: A Small MYC-Binding Compound that Inhibits MYC: MAX Interaction and Tumor Growth in a MYC-Dependent Manner
Authors: Castell Alina , Yan Qinzi , Fawkner Karin , Bazzar Wesam , Zhang Fan , Wickström Malin , Alzrigat Mohammad , Franco Marcela , Krona Cecilia , Cameron Donald P. , Dyberg Cecilia , Olsen Thale Kristin , Verschut Vasiliki , Schmidt Linnéa , Lim Sheryl Y. , Mahmoud Loay , Hydbring Per , Lehmann Sören , Baranello Laura , Nelander Sven , Johnsen John Inge , Larsson Lars-Gunnar
Published: April 2023

Supplementary Figure 1. MYCMI-7 selectively inhibits the MYC:MAX interaction in cells and blocks MYC's association with chromatin. Supplementary Figure 2. MYCMI-7 downregulates MYC and MYCN protein expression. Supplementary Figure 3. MYCMI-7 reduces tumor cell growth/viability of MYC-driven tumor cells and inhibits oncogenic transformation in 2D and 3D cultures. Supplementary Figure 4. Effects of MYCMI-7 is relation to TOP2A activity in vitro and in cells. Supplementary Figure 5. Treatment of MYC/BCL-XL-driven acute myeloid leukemia with MYCMI-7. Supplementary Figure 6. MYCMI-7 inhibits growth of MDA-MB-231 breast cancer cell and SK-N-DZ MYCN-amplified neuroblastoma cell xenografts in vivo.
Supplementary Tables S1-S9 from The Tumor Immune Profile of Murine Ovarian Cancer Models: An Essential Tool for Ovarian Cancer Immunotherapy Research
Authors: Rodriguez Galaxia M. , Galpin Kristianne J.C. , Cook David P. , Yakubovich Edward , Maranda Vincent , Macdonald Elizabeth A. , Wilson-Sanchez Juliette , Thomas Anjali L. , Burdette Joanna E. , Vanderhyden Barbara C.
Published: April 2023

Table S1 contains antibodies used in flow cytometry staining of ascites/PW, spleen, and mouse ovarian tumors.

Table S2 contains primary antibodies used for IHC and IF staining of mouse ovarian tumors.

Table S3 contains primer Sequences used for qPCR of ovarian cancer cell lines.

Table S4 contains hallmark gene list for ID8 and STOSE cancer cells.

Table S5 contains M0/M1/M2 gene-sets.

Table S6 contains tumor development characteristics of murine orthotopic ovarian cancer models.

Table S7 contains average and standard deviation of concentrations of cytokines and chemokines in the ascites of syngeneic mouse models of ovarian cancer at endpoint.

Table S8 contains average and standard deviation of concentrations of cytokines and chemokines in the plasma of syngeneic mouse models of ovarian cancer collected near endpoint.

Table S9 summarizes key features of syngeneic models of ovarian cancer.
Supplementary Figures S1-S13 from The Tumor Immune Profile of Murine Ovarian Cancer Models: An Essential Tool for Ovarian Cancer Immunotherapy Research
Authors: Rodriguez Galaxia M. , Galpin Kristianne J.C. , Cook David P. , Yakubovich Edward , Maranda Vincent , Macdonald Elizabeth A. , Wilson-Sanchez Juliette , Thomas Anjali L. , Burdette Joanna E. , Vanderhyden Barbara C.
Published: April 2023

Figure S1 shows differential gene expression between cancer cell populations of orthotopic ID8-WT and STOSE tumors.

Figure S2 shows UMAP plots of M0/M1/M2 gene set enrichment in ID8-WT and STOSE tumors.

Figure S3 shows expression of MHC-I and PD-L1 under IFNγ treatment in various ovarian cancer cell lines.

Figure S4 shows tumor phenotypes of various murine ovarian cancer models.

Figure S5 shows the gating strategy for analysis of flow cytometry data.

Figure S6 shows abundance of T cell populations in the TME of syngeneic ovarian cancer models.

Figure S7 shows abundance of myeloid-like cell populations in the TME of various syngeneic ovarian cancer models.

Figure S8 shows MHC-II expression in immune and stromal compartments of orthotopic tumors from syngeneic ovarian cancer models.

Figure S9 shows PD-L1 expression in immune and stromal compartments of orthotopic tumors from syngeneic ovarian cancer models.

Figure S10 shows relative immune cell frequencies found in spleens of ovarian tumor-bearing mice.

Figure S11 shows MHC-II and PD-L1 expression in the TME and ascites of ovarian tumor-bearing mice.

Figure S12 shows the chemokine and cytokine network found in the ascites and plasma of ovarian tumor-bearing mice.

Figure S13 shows chemokine and cytokine expression from single-cell RNA-sequencing analysis of ID8 and STOSE tumors.
Supplemental Table 7 from Race-associated Molecular Changes in Gynecologic Malignancies
Authors: Asare Amma , Yao Hui , Lara Olivia D. , Wang Ying , Zhang Lin , Sood Anil K.
Published: April 2023

Differentially methylated probes identified independently in epigenetic studies of environment
Supplementary Tables 1-3, Figures 1-4 from Redirecting T-cell Activity with Anti-BCMA/Anti-CD3 Bispecific Antibodies in Chronic Lymphocytic Leukemia and Other B-cell Lymphomas
Authors: Martens Anne W.J. , Rietveld Joanne M. , de Boer Renate , Peters Fleur S. , Ngo An , van Mil Lotte W.H.G. , de Heer Koen , Spaargaren Marcel , Verkleij Christie P.M. , van de Donk Niels W.C.J. , Adams Homer C. , Eldering Eric , van Noesel Carel J.M. , Verona Raluca , Kater Arnon P.
Published: April 2023

Supplementary Table 1. CLL Patient characteristics. Supplementary Table 2. Healthy donor characteristics. Supplementary Table 3. MM patient characteristics. Supplementary Figure 1. γ-secretase inhibition increases BCMA levels but does not affect viability of B-cell malignancy cell lines. Supplementary Figure 2. γ-secretase inhibition does not affect viability CLL cells. Supplementary Figure 3. BCMAxCD3 DuoBody® induces activation, degranulation, and cytokine secretion by T cells in the presence of B cell malignancy cell lines. Supplementary Figure 4. BCMAxCD3 DuoBody® induces autologous killing of MM cells.
Supplemental Table 3 from Race-associated Molecular Changes in Gynecologic Malignancies
Authors: Asare Amma , Yao Hui , Lara Olivia D. , Wang Ying , Zhang Lin , Sood Anil K.
Published: April 2023

Gene Set Enrichment Analysis of transcriptional changes in AA samples
Supplemental Figure S4 from Race-associated Molecular Changes in Gynecologic Malignancies
Authors: Asare Amma , Yao Hui , Lara Olivia D. , Wang Ying , Zhang Lin , Sood Anil K.
Published: April 2023

Analysis of methylation changes by tumor type
Supplemental Figure S1 from Race-associated Molecular Changes in Gynecologic Malignancies
Authors: Asare Amma , Yao Hui , Lara Olivia D. , Wang Ying , Zhang Lin , Sood Anil K.
Published: April 2023

Detailed patient racial assignments by tumor type and additional pathway analysis
Supplementary Tables S1-S4 from Serum Carotenoids and Cancer-Related Fatigue: An Analysis of the 2005–2006 National Health and Nutrition Examination Survey
Authors: Kleckner Amber S. , van Wijngaarden Edwin , Jusko Todd A. , Kleckner Ian R. , Lin Po-Ju , Mustian Karen M. , Peppone Luke J.
Published: April 2023

Suppl. Table 1. Results of crude and adjusted models describing the association between carotenoid concentrations and fatigue: all model output. For body mass index, estimates are compared to normal weight (18.5-<25 kg/m2); 1=<18.5 kg/m2, 3=25-<30 kg/m2, and 4=≥30 kg/m2). For race/ethnicity, estimates are compared to non-Hispanic White, 1=Mexican American, 2=Other Hispanic, 4=non-Hispanic Black American, 5=Other non-Hispanic race, including multi-racial. For education, estimates are compared to having at least a college education (11= less than a high school education, 12= at least high school but less than a four-year college education, 13=at least a four-year college education).

Suppl. Table 2. Results of adjusted model with the nutrient×cancer interaction term to explore the associations between carotenoids and cancer-related fatigue: all model output.

Suppl. Table 3. Adjusted odds ratios and 95% confidence intervals for the effects of the nutrient×cancer interaction on fatigue. Models are adjusted for age, body mass index, race/ethnicity, education, physical activity, history of a cancer diagnosis, and nutrient concentration.

Suppl. Table 4. Results of adjusted models (no interaction term) describing the association between carotenoid concentrations and fatigue only among cancer survivors: all model output; estimates for race/ethnicity are compared to non-Hispanic Whites, 1=Mexican American, 2=Other Hispanic, 4=non-Hispanic Black American, 5=Other non-Hispanic race, including multi-racial; estimates for body mass index are compared to those of normal weight; and estimates for education are compared to those with at least a college education. Exercise is estimated from metabolic equivalents (MET hours) per week as a continuous variable. Age, Years since Diagnosis, and carotenoid concentration are treated as continuous variables. (n=272)
Supplementary Table S2 from Development of an Automated Liquid Biopsy Assay for Methylated Markers in Advanced Breast Cancer
Authors: Fackler Mary Jo , Tulac Suzana , Venkatesan Neesha , Aslam Adam J. , de Guzman Timothy N. , Mercado-Rodriguez Claudia , Cope Leslie M. , Downs Bradley M. , Vali Abdul Hussain , Ding Wanjun , Lehman Jennifer , Denbow Rita , Reynolds Jeffrey , Buckley Morgan E. , Visvanathan Kala , Umbricht Christopher B. , Wolff Antonio C. , Stearns Vered , Bates Michael , Lai Edwin W. , Sukumar Saraswati
Published: April 2023

The table provides a step by step guide to calculate methylation in each gene followed by cumulative methylation using the algorithm derived in this paper.
Supplementary Table S1 from Development of an Automated Liquid Biopsy Assay for Methylated Markers in Advanced Breast Cancer
Authors: Fackler Mary Jo , Tulac Suzana , Venkatesan Neesha , Aslam Adam J. , de Guzman Timothy N. , Mercado-Rodriguez Claudia , Cope Leslie M. , Downs Bradley M. , Vali Abdul Hussain , Ding Wanjun , Lehman Jennifer , Denbow Rita , Reynolds Jeffrey , Buckley Morgan E. , Visvanathan Kala , Umbricht Christopher B. , Wolff Antonio C. , Stearns Vered , Bates Michael , Lai Edwin W. , Sukumar Saraswati
Published: April 2023

Table contains sequences of primers and probes used to amplify the nine markers and ACTB in the LBx-BCM assay
Supplementary Fig S5 from Development of an Automated Liquid Biopsy Assay for Methylated Markers in Advanced Breast Cancer
Authors: Fackler Mary Jo , Tulac Suzana , Venkatesan Neesha , Aslam Adam J. , de Guzman Timothy N. , Mercado-Rodriguez Claudia , Cope Leslie M. , Downs Bradley M. , Vali Abdul Hussain , Ding Wanjun , Lehman Jennifer , Denbow Rita , Reynolds Jeffrey , Buckley Morgan E. , Visvanathan Kala , Umbricht Christopher B. , Wolff Antonio C. , Stearns Vered , Bates Michael , Lai Edwin W. , Sukumar Saraswati
Published: April 2023

Figure shows changes in LBx-BCM methylation in response to chemotherapy in 7 additional patient longitudinal serial samples. LBx-BCM was performed and cumulative methylation (CM) (Y-axis) is plotted from serum samples drawn at baseline (0 days) and immediately before each treatment cycle (X-axis). For each patient, treatment cycles are shown as a shaded area. PD, progressive disease; SD, stable disease (SD).
Supplementary Fig S3 from Development of an Automated Liquid Biopsy Assay for Methylated Markers in Advanced Breast Cancer
Authors: Fackler Mary Jo , Tulac Suzana , Venkatesan Neesha , Aslam Adam J. , de Guzman Timothy N. , Mercado-Rodriguez Claudia , Cope Leslie M. , Downs Bradley M. , Vali Abdul Hussain , Ding Wanjun , Lehman Jennifer , Denbow Rita , Reynolds Jeffrey , Buckley Morgan E. , Visvanathan Kala , Umbricht Christopher B. , Wolff Antonio C. , Stearns Vered , Bates Michael , Lai Edwin W. , Sukumar Saraswati
Published: April 2023

Figure shows the perfomance of LBx-BCM in the training set samples. A histogram shows cumulative methylation for each sample, and a box plot shows significnt difference of methylation in serum of metastatic breast cancer patients compared to normal individuals (Mann Whitney p= 0.002)
Supplementary Fig S1 from Development of an Automated Liquid Biopsy Assay for Methylated Markers in Advanced Breast Cancer
Authors: Fackler Mary Jo , Tulac Suzana , Venkatesan Neesha , Aslam Adam J. , de Guzman Timothy N. , Mercado-Rodriguez Claudia , Cope Leslie M. , Downs Bradley M. , Vali Abdul Hussain , Ding Wanjun , Lehman Jennifer , Denbow Rita , Reynolds Jeffrey , Buckley Morgan E. , Visvanathan Kala , Umbricht Christopher B. , Wolff Antonio C. , Stearns Vered , Bates Michael , Lai Edwin W. , Sukumar Saraswati
Published: April 2023

Figure shows the relationship between PCR Cycle threshold (Ct) and target DNA copy (0-300 copies) input
Table S7 from A Phenogenetic Axis that Modulates Clinical Manifestation and Predicts Treatment Outcome in Primary Myeloid Neoplasms
Authors: Shen Qiujin , Feng Yahui , Gong Xiaowen , Jia Yujiao , Gao Qingyan , Jiao Xiaokang , Qi Saibing , Liu Xueou , Wei Hui , Huang Bingqing , Zhao Ningning , Song Xiaoqiang , Ma Yueshen , Liang Shihao , Zhang Donglei , Qin Li , Wang Ying , Qu Shiqiang , Zou Yao , Chen Yumei , Guo Ye , Yi Shuhua , An Gang , Jiao Zengtao , Zhang Song , Li Linfeng , Yan Jun , Wang Huijun , Song Zhen , Mi Yingchang , Qiu Lugui , Zhu Xiaofan , Wang Jianxiang , Xiao Zhijian , Chen Junren
Published: April 2023

Table S7. Prevalence of chromosomal abnormalities in THAMP.