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Defining 2 biologically and clinically distinct groups in acute leukemia with a mixed phenotype

Blood 2025年第18期145卷 2056-2069页

作者： Galera, Pallavi Dilip, Deepika Derkach, Andriy Chan, Alexander Zhang, Yanming Persaud, Sonali Mishra, Tanmay Kramer, Kyle Kathpalia, Mahak Liu, Ying Famulare, Christopher Gao, Qi Mata, Douglas A. Arcila, Maria Geyer, Mark B. Stein, Eytan Dogan, Ahmet Roshal, Mikhail Levine, Ross L. Glass, Jacob Xiao, Wenbin Hematopathology Service Department of Pathology and Laboratory Medicine Memorial Sloan Kettering Cancer Center New York NY United States Center for Epigenetics Research Memorial Sloan Kettering Cancer Center New York NY United States Department of Epidemiology and Biostatistics Memorial Sloan Kettering Cancer Center New York NY United States Department of Pathology and Laboratory Medicine Cytogenetics Laboratory Memorial Sloan Kettering Cancer Center New York NY United States Molecular Cancer Medicine Service Human Oncogenesis and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York NY United States Department of Pathology and Laboratory Medicine Diagnostic Molecular Laboratory Memorial Sloan Kettering Cancer Center New York NY United States Center for Hematologic Malignancies Memorial Sloan Kettering Cancer Center New York NY United States Leukemia Service Department of Medicine Memorial Sloan Kettering Cancer Center New York NY United States Cell Therapy Service Department of Medicine Memorial Sloan Kettering Cancer Center New York NY United States

A mixed phenotype (MP) is a characteristic of de novo MP acute leukemia (MPAL), but it can also be found in other leukemias. It poses substantial classification and management dilemmas. Herein, we report a large cohort of acute leukemia with MP and define acute myeloid leukemia with MP (AML-MP) and MPAL as 2 distinct groups by characterizing clinical, genetic, and transcriptomic features. Clinically, patients with AML-MP and MPAL were both treated with either AML- or acute lymphoblastic leukemia (ALL)–directed induction regimens. AML-MP has inferior responses (hazard ratio, 12.5;95% confidence interval, 2.72-57.8;P = .001), whereas MPAL has better responses to ALL-directed treatment. Genetically, AML-MP harbors more frequent RUNX1 (23/52 [44%]) and TP53 (12/52 [23.1%]) mutations. In contrast, RUNX1 mutations are less frequent in MPAL (8/35 [23%];P = .01 vs AML-MP) and TP53 mutations as a driver are virtually absent in MPAL. Transcriptionally, AML-MP shows enrichment for stemness signatures and a relative deficit of transcription factors critical for myeloid and lymphoid differentiation. Furthermore, AML-MP rarely switches to a lymphoid immunophenotype after treatment, in contrast to MPAL (1/40 [2.5%] vs 10/28 [35.7%];P = .0003). Last, a genomic classification framework is proposed for future studies. Together, these data support the designation of AML-MP as a diagnosis distinct from MPAL and provide novel insights into the pathogenesis and therapies of acute leukemia with MP. © 2025 American Society of Hematology

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SETD2-linking stem cell survival and transformation

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细胞研究（英文版） 2018年第4期28卷 393-394页

作者： Mrinai M. Patnaik Omar Abdel-Wahab Department of Internal Medicine Mayo Clinic Division of Hematology Rochester MN USA Human Oncology and Pathogenesis Program and Acute Leukemia Service Memorial Sloan Kettering Cancer Center New York NY 10065 USA

SETD2 encodes a histone H3 lysine 36 (H3K36) methyltrans-ferase affected by mutations and deletions in a wide variety of cancers. Whether SETD2 loss alone can initiate tumorigenesis has not been established previously but in the present study, Zhang et al. identify that SETD2 deficiency eventually results in outgrowth of cells with a phenotype consistent with myelodysplastic syndromes and acute myeloid *** modifications of histones are important regulators of gene expression with H3K36me3 being tightly associated with transcriptionally active regions of chromatin and gene bodies.1 SETD2 is the sole H3K36 trimethyltransferase in eukaryotic cells and SETD2 has been ascribed to be involved in a number of biological processes mediated by diverse proteins with H3K36me3 reader domains (reviewed recently).2 This includes a role for SETD2 in DNA mismatch repair (through H3K36me3 binding of the protein hMS6), homologous recombination (mediated by LEDGF), DNA methylation (through H3K36me3 binding of DNMT3B), and nucleosome reorganization (through binding of the FACT complex to H3K36me3). Moreover, SETD2 itself physically associates with the hyperphosphorylated C-terminal domain of RNA polymerase II(RNA pol II), an association thought to link H3K36 trimethylation to sites of active transcription. The association between SETD2 and transcription has been shown to provide an indirect role for SETD2 in regulating RNA splicing, which is performed in a cotranscriptional manner and influenced by RNA pol II elongation at certain loci.

关键词： Cancer models Haematopoietic stem cells Mechanisms of disease

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Redifferentiation therapy in unresectable or metastatic radioactive iodine refractory thyroid cancer: an International Thyroid oncology Group statement

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The Lancet Diabetes and Endocrinology 2025年第6期13卷 516-527页

作者： Leboulleux, Sophie Boucai, Laura Busaidy, Naifa Durante, Cosimo Fagin, James A Fazeli, Sasan Gianoukakis, Andrew G Haugen, Bryan R Kang, Hyunseok Konda, Bhavana Laetsch, Theodore W Locati, Laura Ryder, Mabel Spitzweg, Christine Worden, Francis P Wirth, Lori Ho, Alan Department of Medicine Endocrinology and Diabetology Service Geneva University Hospitals and Univerisity of Geneva Geneva Switzerland Department of Medicine Endocrinology Service Memorial Sloan Kettering Cancer Center New York NY United States Department of Endocrine Neoplasia and Hormonal Disorders The University of Texas MD Anderson Cancer Center Houston TX United States Department of Translational and Precision Medicine Sapienza University of Rome Rome Italy Department of Medicine Memorial Sloan Kettering Cancer Center New York NY United States Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York NY United States Department of Clinical Diabetes Endocrinology & Metabolism City of Hope Comprehensive Cancer Center Duarte CA United States Division of Endocrinology Diabetes and Metabolism David Geffen School of Medicine at UCLA Harbor-UCLA Medical Center Los Angeles CA United States Division of Endocrinology Metabolism and Diabetes University of Colorado School of Medicine Aurora CO United States Department of Medicine University of California at San Francisco San Francisco CA United States Division of Medical Oncology Department of Internal Medicine The Ohio State University Comprehensive Cancer Center Columbus OH United States Center for Childhood Cancer Research Children's Hospital of Philadelphia Philadelphia PA United States Medical Oncology Unit Istituti Clinici Scientifici Maugeri IRCCS Pavia Italy Division of Endocrinology Diabetes Metabolism and Nutrition Mayo Clinic Rochester MN United States Department of Internal Medicine IV LMU Munich Germany Division of Endocrinology Diabetes Metabolism and Nutrition Mayo Clinic Rochester Minnesota United States Department of Internal Medicine Division of Hematology and Oncology University of Michigan Rogel Cancer Center Ann Arbor MI United States Harvard Medical School Boston MA United States Center for Head and Neck Cancers Massachusetts General Hospital

In patients with follicular cell-derived thyroid cancer that have distant metastases and no iodine uptake, redifferentiation—ie, the restoration of tumoural 131I uptake with systemic therapy—is now possible. The use...

In patients with follicular cell-derived thyroid cancer that have distant metastases and no iodine uptake, redifferentiation—ie, the restoration of tumoural ¹³¹I uptake with systemic therapy—is now possible. The use of mitogen-activated protein kinase (MAPK) inhibitors for a short period of time before the administration of high activity ¹³¹I shows promising results with iodine uptake restoration and tumour response. Redifferentiation has been used in patients with BRAF-mutated and RAS-mutated tumours in prospective trials and in the case of patients with RET or NTRK fusions. The iodine uptake restoration ranges from 33% to 95%, and tumour response rates from 11% to 80%. There is substantial variability between trials with regards to inclusion criteria, duration of redifferentiation drug therapy, activity of radioactive iodine, and use of dosimetry. Randomised studies are missing to clearly establish the effectiveness and applicability of redifferentiation. Thus, long-term studies are needed to establish the most effective redifferentiation protocols. The objectives of this Review are to: (1) provide a comprehensive review of the available results from prospective trials and case reports, including results regarding the restoration of radioiodine uptake and treatment efficacy (morphological and biological);(2) describe the differences in redifferentiation trial design between studies and discuss their potential impact on treatment efficacy;(3) describe the implications and limitations of dosimetry;and (4) outline the key questions to be addressed in future redifferentiation trials. © 2025 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license

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LSD1 Inhibitor CPI-482 Shows Efficacy and Prolongs Survival in Mouse Models of AML and Post-MPN AML in the Context of Constitutive JAK-STAT Pathway Activation

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BLOOD 2020年 136卷 50-51页

作者： Rampal, Raajit K. McGrath, John P. Krishnan, Aishwarya Li, Bing Xiao, Wenbin Nikom, David Wang, Jing Levine, Ross L. Trojer, Patrick Leukemia Service Department of Medicine Memorial Sloan Kettering Cancer Center New York NY Translational Sciences Constellation Pharmaceuticals Cambridge MA Center for Hematologic Malignancies Memorial Sloan Kettering Cancer Center New York NY Department of Pathology Memorial Sloan Kettering Cancer Center New York NY Constellation Pharmaceuticals Cambridge MA Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York NY Department of Medicine Leukemia Service Memorial Sloan Kettering Cancer Center New York NY

Several novel mechanism-based therapeutic modalities are currently being clinically investigated for the treatment of patients with acute myelogenous leukemia (AML), including agents that exploit genomic vulnerabilities, attenuate leukemia stem cell populations and/or or synergize with anti-leukemic cytotoxic/epigenetic therapies. Lysine-specific demethylase 1 (LSD1) is an enzyme that functions in transcriptional repression by catalyzing the removal of histone H3 lysine 4 methylation, a histone modification associated with transcriptionally competent gene enhancers and transcriptional start sites. Small molecule mediated inhibition of LSD1 alters the chromatin state and the transcriptional output of LSD1 target genes. Transcriptional ‘reprogramming’ by LSD1 inhibitors either causes a direct impact on cell fate and/or renders malignant cells more susceptible to the treatment with other cancer therapeutic agents. LSD1 inhibitors have shown encouraging phenotypic effects in myelogenous leukemia (AML) models but the key molecular determinants governing LSD1 inhibitor sensitivity remain to be further investigated. Here, we explored the in vitro sensitivity of 350 cancer cell lines to our LSD1 inhibitor CPI-482 to identify potential hyper-responder cell contexts. Four AML cell lines showed high sensitivity with low nanomolar concentration GI 50 s, each of which contained either a JAK2 V617F mutation or a genetic aberration that resulted in JAK-STAT pathway activation. Oral administration of LSD1 inhibitor CPI-482 on a once daily or a once weekly dosing schedule resulted in significant tumor growth inhibition in SET-2 and HEL 92.1.7 JAK2 mutant AML xenograft mouse models. Given the unmet need and poor prognosis in post-MPN secondary AML (sAML) we then explored CPI-482 in a tertiary transplant post-MPN AML retroviral transduction murine model ( Jak2 V617F retrovirus transduced into Tp53 null bone marrow). Jak2 V617F/ Tp53 null spleen cells were transplanted into lethally ir

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Treatment breakthroughs for the management of acute myeloid leukemia

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International Journal of Hematologic oncology 2012年第2期1卷 121-132页

作者： Justin M Watts Ross L Levine Martin S Tallman Leukemia Service Department of Medicine Memorial Sloan–Kettering Cancer Center New York NY USA Human Oncology & Pathogenesis Program Leukemia Service Department of Medicine Memorial Sloan–Kettering Cancer Center New York NY USA Leukemia Service Department of Medicine Memorial Sloan–Kettering Cancer Center New York NY USA.

SUMMARY Although there has been substantial improvement in the survival of younger patients with acute myeloid leukemia (AML) since the 1970s, over the past two decades subsequent gains have been modest. Survival rates in older patients with AML remain dismal and have seen minimal change since the advent of modern induction chemotherapy. However, over the past decade, there has been a dramatic increase in the development of new therapies that have promising potential to further improve survival in both older and younger patients with AML. In this review, we will examine recent and ongoing breakthroughs in genetic discovery and gene profiling, intensification of induction chemotherapy, the development of novel agents, the management of older adults and allogeneic hematopoietic cell transplantation. We will also discuss exciting advances in the management of acute promyelocytic leukemia; a disease that is now imminently curable.

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Venetoclax Therapy for Relapsed and Treatment Refractory AML: Clinical Outcomes and Molecular Predictors

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BLOOD 2020年 136卷 47-48页

作者： Stahl, Maximilian Menghrajani, Kamal Derkach, Andriy Chan, Alexander Xiao, Wenbin Glass, Jacob L. King, Amber C. Daniyan, Anthony Famulare, Christopher Cuello, Bernadette M. Abdel-Wahab, Omar Levine, Ross L. Viny, Aaron D. Stein, Eytan M. Roshal, Mikhail Tallman, Martin S. Goldberg, Aaron D. Department of Medicine Leukemia Service Memorial Sloan Kettering Cancer Center New York NY Weill Cornell Medical College New York NY Department of Biostatistics and Epidemiology Memorial Sloan Kettering Cancer Center New York NY Department of Pathology Memorial Sloan Kettering Cancer Center New York NY Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York Center for Epigenetics Research Memorial Sloan Kettering Cancer Center New York NY Department of Pharmacy Memorial Sloan Kettering Cancer Center New York NY Department of Medicine Leukemia Service Memorial Sloan Kettering Cancer Center NY NY Center for Hematologic Malignancies Memorial Sloan Kettering Cancer Center New York NY Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York NY Memorial Sloan-Kettering Cancer Center New York NY Department of Medicine Leukemia Service Memorial Sloan-Kettering Cancer Center New York NY

Background: Venetoclax combined with azacitidine (aza/ven), decitabine (dec/ven), and low-dose cytarabine (LDAC/ven) is commonly used off-label in relapsed/refractory (RR)-AML patients; however, predictors of response and survival are incompletely understood. Objectives: To report clinical outcomes of RR-AML patients (pts) treated with venetoclax combination therapy and to analyze molecular predictors of these outcomes. Methods: All pts with RR-AML, who received treatment with aza/ven, dec/ven or LDAC/ven from 08/2016 to 02/2020 at Memorial Sloan Kettering Cancer Center in New York City were included. The best response to therapy was determined using the 2017 European leukemiaNet (ELN) response criteria. The overall response rate (ORR) was defined as the combination of the complete response (CR) + complete response with incomplete count recovery (CRi) + morphologic leukemia free state (MLFS) rate. Measurable residual disease (MRD) was assessed by multiparameter flow cytometric analysis of bone marrow aspirate samples and any level of residual disease was considered MRD+. Overall survival (OS) was calculated from cycle 1 day 1 of therapy until death or time of last follow-up. Results: A total of 86 pts were treated with venetoclax-based combination therapy ( A ). Median age was 67 years. More than half of the pts had received prior HMA therapy, 17% had received a prior allogeneic stem cell transplant. The majority of pts received aza/ven (41%) while 23% and 31% received dec/ven and LDAC/ven, respectively. Treatment trajectories of all patients are shown in the Swimmers' plot in panel ( B ). While the ORR was 31% and 24% of patients achieved a CR/CRi, 60% of pts were refractory to venetoclax therapy; 45% of responding pts eventually relapsed with a median follow up of 12 months ( B, C ). Oncoprint showing associations between molecular patterns and response to venetoclax combination therapy is shown in panel ( D ). Mutations in NPM1 (CR/CRi 46%, ORR 62%; OR 4.53, 95%

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Management of patients with advanced-stage HER2-positive breast cancer: current evidence and future perspectives (vol 21, pg 185, 2024)

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NATURE REVIEWS CLINICAL oncology 2024年第9期21卷 701-701页

作者： Marra, Antonio Chandarlapaty, Sarat Modi, Shanu Division of New Drugs and Early Drug Development European Institute of Oncology IRCCS Milan Italy Human Oncology and Pathogenesis Program (HOPP) Memorial Sloan Kettering Cancer Center New York NY USA Breast Medicine Service Department of Medicine Memorial Sloan Kettering Cancer Center New York NY USA Weill Cornell Medical College New York NY USA

Amplification and/or overexpression of ERBB2, the gene encoding HER2, can be found in 15–20% of invasive breast cancers and is associated with an aggressive phenotype and poor clinical outcomes. Relentless research efforts in molecular biology and drug development have led to the implementation of several HER2-targeted therapies, including monoclonal antibodies, tyrosine-kinase inhibitors and antibody–drug conjugates, constituting one of the best examples of bench-to-bedside translation in oncology. Each individual drug class has improved patient outcomes and, importantly, the combinatorial and sequential use of different HER2-targeted therapies has increased cure rates in the early stage disease setting and substantially prolonged survival for patients with advanced-stage disease. In this Review, we describe key steps in the development of the modern paradigm for the treatment of HER2-positive advanced-stage breast cancer, including selecting and sequencing new-generation HER2-targeted therapies, and summarize efficacy and safety outcomes from pivotal studies. We then outline the factors that are currently known to be related to resistance to HER2-targeted therapies, such as HER2 intratumoural heterogeneity, activation of alternative signalling pathways and immune escape mechanisms, as well as potential strategies that might be used in the future to overcome this resistance and further improve patient outcomes.

关键词： Breast cancer Targeted therapies Tumour biomarkers

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BRAFV600E Mutations Occur In The Hematopoietic Stem Cell Compartment In Hairy Cell leukemia

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BLOOD 2013年第21期122卷 816-816页

作者： Chung, Stephen S. Park, Jae H. Kim, Eunhee Chung, Young Rock Hu, Wenhuo Lito, Piro Feldstein, Julie Teruya Rampal, Raajit K. Telis, Leon Patel, Minal Rosen, Neal Park, Christopher Y. Tallman, Martin S. Abdel-Wahab, Omar Leukemia Service Department of Medicine Memorial Sloan-Kettering Cancer Center New York NY USA Human Oncology and Pathogenesis Program Memorial Sloan-Kettering Cancer Center New York NY USA Leukemia Service and Human Oncology and Pathogenesis Program Memorial Sloan-Kettering Cancer Center New York City NY USA Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York NY USA Pharmacology Memorial Sloan-Kettering Cancer Center New York USA Department of Pathology Memorial Sloan-Kettering Cancer Center New York NY USA Human Oncology and Pathogenesis Program and Leukemia Service Memorial Sloan-Kettering Cancer Center New York NY USA Human Oncology and Pathogenesis Program Memorial Sloan-Kettering Cancer Center New York USA Medicine Memorial Sloan-Kettering Cancer Center New York USA Pathology and Human Oncology and Pathogenesis Program Memorial Sloan-Kettering Cancer Center New York NY USA

816

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Identification Of Actionable Genomic Alterations In Hematologic Malignancies By a Clinical Next Generation Sequencing-Based Assay

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BLOOD 2013年第21期122卷 230-230页

作者： Lipson, Doron Nahas, Michelle K. Otto, Geoff A. Yelensky, Roman Abdel-Wahab, Omar Wang, Kai He, Jie Intlekofer, Andrew M. Rampal, Raajit K. Brennan, Timothy A. Knapp, Kristina M. Brennan, Kristina W. Young, Geneva Donahue, Amy L. Sanford, Eric M. Greenbowe, Joel R. Frampton, Garrett M. Fichtenholtz, Alex Young, Lauren E. Erlich, Rachel L. Parker, Alex Klimstra, David Dogan, Ahmet Ross, Jeffrey S. Armstrong, Scott A. Stephens, Philip J. van den Brink, Marcel R. M. Miller, Vincent A. Levine, Ross L. Foundation Medicine Inc Cambridge MA USA Leukemia Service and Human Oncology and Pathogenesis Program Memorial Sloan-Kettering Cancer Center New York City NY USA Department of Medicine Memorial Sloan-Kettering Cancer Center New York NY USA Human Oncology and Pathogenesis Program and Leukemia Service Memorial Sloan-Kettering Cancer Center New York NY USA

230

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ZRSR2 Mutation Induced Minor Intron Retention Drives MDS and Diverse Cancer Predisposition Via Aberrant Splicing of LZTR1

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BLOOD 2020年 136卷 10-11页

作者： Inoue, Daichi Polaski, Jacob T. Taylor, Justin Castel, Pau Chen, Sisi Kobayashi, Susumu Hogg, Simon J. Hayashi, Yasutaka Pineda, Jose Mario Bello Penson, Alexander V. El Marabti, Ettaib Erickson, Caroline Fukumoto, Miki Yamazaki, Hiromi Fukui, Chie Lu, Sydney X. Durham, Benjamin H. Liu, Bo Mehta, Sanjoy Zakheim, Daniel Garippa, Ralph Chew, Guo-Liang McCormick, Frank Bradley, Robert K. Abdel-Wahab, Omar Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York NY Department of Hematology-Oncology Institute of Biomedical Research and Innovation Foundation for Biomedical Research and Innovation at Kobe Kobe Japan Public Health Sciences and Basic Sciences Divisions Fred Hutchinson Cancer Research Center Seattle Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center Miami FL Helen Diller Family Comprehensive Cancer Center University of California San Francisco San Francisco Foundation for Biomedical Research and Innovation at Kobe Kobe Japan Department of Genome Sciences University of Washington Seattle Memorial Sloan Kettering Cancer Center New York Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York Myeloma Service Department of Medicine Memorial Sloan Kettering Cancer Center New York NY Gene Editing & Screening Facility Memorial Sloan Kettering Cancer Center New York

Mutations in RNA splicing factors are amongst the most common genetic alterations in myeloid malignancies. Mutations in the splicing factors SF3B1 , SRSF2 , and U2AF1 occur as heterozygous, missense mutations and have been shown to confer a change-of-function. In contrast, the X chromosome encoded ZRSR2 is enriched in nonsense/frameshift mutations in males, consistent with loss of function. To date however, we do not understand the basis for enrichment of ZRSR2 mutations in leukemia. Moreover, ZRSR2 is the only one of these factors that primarily functions in the minor spliceosome. While most introns are spliced by the major spliceosome, a small subset (<1%) of introns are recognized by a separate complex, the minor spliceosome. Although minor (or “U12”) introns are present in only ~800 genes in humans, their sequences and positions are highly evolutionarily conserved - more so than their U2 counterparts. The high conservation of minor introns suggests key regulatory roles yet few functional roles for the minor spliceosome in regulating biological phenotypes are known. The rarity and conservation of minor introns offered a unique opportunity to investigate splicing factor mutations and identify potential tissue-specific roles of the minor spliceosome. Modeling loss-of-function mutations in ZRSR2 via a mouse model for induced deletion of Zrsr2 revealed strikingly enhanced self-renewal of Zrsr2 -deficient male and female hematopoietic cells ( Fig. A-C ). This was in stark contrast to the effects of hotspot mutations in Sf3b1 and Srsf2 and similar to those of Tet2 loss on increasing self-renewal and numbers of HSCs. Zrsr2 loss was also associated increased myeloid cells in the blood and long-term hematopoietic stem cells (HSCs) in the marrow ( Fig. C ). To understand the mechanistic basis by which ZRSR2 loss causes aberrant HSC self-renewal, we quantified transcriptome-wide splicing patterns in MDS patients. ZRSR2 -mutant samples had widespread, dysfunctional recogniti

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