Leukemia最新文献

{"title":"The protein deacetylase HDAC10 controls DNA replication in malignant lymphoid cells","authors":"Andreas O. Mieland, Giuseppe Petrosino, Mario Dejung, Jia-Xuan Chen, Amitkumar Fulzele, Fereshteh Mahmoudi, Jia-Wey Tu, Al-Hassan M. Mustafa, Yanira Zeyn, Christoph Hieber, Matthias Bros, Tina M. Schnöder, Florian H. Heidel, Sara Najafi, Ina Oehme, Ilse Hofmann, Mike Schutkowski, Sebastian Hilscher, Christian Kosan, Falk Butter, Sanil Bhatia, Wolfgang Sippl, Oliver H. Krämer","doi":"10.1038/s41375-025-02612-8","DOIUrl":"https://doi.org/10.1038/s41375-025-02612-8","url":null,"abstract":"<p>Histone deacetylases (HDACs) comprise a family of 18 epigenetic modifiers. The biologically relevant functions of HDAC10 in leukemia cells are enigmatic. We demonstrate that human cultured and primary acute B cell/T cell leukemia and lymphoma cells require the catalytic activity of HDAC10 for their survival. In such cells, HDAC10 controls a MYC-dependent transcriptional induction of the DNA polymerase subunit POLD1. Consequently, pharmacological inhibition of HDAC10 causes DNA breaks and an accumulation of poly-ADP-ribose chains. These processes culminate in caspase-dependent apoptosis. PZ48 does not damage resting and proliferating human normal blood cells. The in vivo activity of PZ48 against ALL cells is verified in a <i>Danio rerio</i> model. These data reveal a nuclear function for HDAC10. HDAC10 controls the MYC-POLD1 axis to maintain the processivity of DNA replication and genome integrity. This mechanistically defined “HDAC10ness” may be exploited as treatment option for lymphoid malignancies.</p><figure></figure>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"18 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143884656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sulforaphane promotes natural killer cell-mediated anti-tumor immune responses partially via cGAS-STING pathway in classical Hodgkin lymphoma","authors":"Ioanna Xagoraris, Ying Yang, Erofili Bougka, Dora Trogrlic, Persa Xyderou, Konstantina Stathopoulou, Nikolas Herold, Andreas Lundqvist, George Z. Rassidakis","doi":"10.1038/s41375-025-02627-1","DOIUrl":"https://doi.org/10.1038/s41375-025-02627-1","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"153 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143880344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic impact of clonal representation of myelodysplasia-related gene mutations in acute myeloid leukemia","authors":"Rabea Mecklenbrauck, Nora Borchert, Razif Gabdoulline, Piroska Poll, Carolin Funke, Maximilian Brandes, Louisa-Kristin Dallmann, Walter Fiedler, Jürgen Krauter, Arne Trummer, Bernd Hertenstein, Martin Müller, Michael Lübbert, Monika Schwalenberg, Andreas Voss, Nataliya Di Donato, Anke Bergmann, Verena Gaidzik, Konstanze Döhner, Hartmut Döhner, Arnold Ganser, Florian H. Heidel, Felicitas R. Thol, Michael Heuser","doi":"10.1038/s41375-025-02622-6","DOIUrl":"https://doi.org/10.1038/s41375-025-02622-6","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"35 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143880348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Wnt5a induces ROR1 dependent NF-κB activation to enhance MMP-9 expression and invasiveness in chronic lymphocytic leukemia","authors":"Md Kamrul Hasan, George F. Widhopf II, Emanuela M. Ghia, Thomas J. Kipps","doi":"10.1038/s41375-025-02616-4","DOIUrl":"https://doi.org/10.1038/s41375-025-02616-4","url":null,"abstract":"<p>Matrix metalloproteinase-9 (MMP-9) facilitates the extravasation and lymphoid-tissue infiltration of chronic lymphocytic leukemia (CLL) cells. Prior studies found that high level expression of MMP-9 in CLL associates more aggressive disease. We find that circulating CLL cells that express high levels the onco-embryonic protein ROR1 express significantly higher levels of MMP-9. Stimulation of CLL cells with Wnt5a could enhance expression and the release of MMP-9 into the culture media and increase the capacity of CLL cells to invade Matrigel in a Boyden-Chamber Assay. Such effects of Wnt5a could not be inhibited by BTK inhibitors such as ibrutinib or zanubrutinib, but could be blocked by zilovertamab, a humanized mAb specific for ROR1. We found that siRNA silencing of NF-κB-p65 or use of an NF-κB inhibitor (CAS 545380-34-5) blocked the capacity of Wnt5a to induce MMP-9 or enhance the invasive capacity of treated CLL cells. Moreover, siRNA directed silencing of <i>MMP9</i> or treatment with an MMP-9 inhibitor (CAS 1177749-58-4) also blocked the invasive capability of CLL cells induced by Wnt5a. We conclude that Wnt5a-induced ROR1-signaling can induce expression of MMP-9 on CLL cells through activation of NF-κB, thereby enhancing the extravasation and lymphoid-tissue infiltration required for CLL cell trafficking.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"91 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143880471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Somatic mutations and outcomes in chronic myeloid leukemia adolescent and young adults compared to children, adults, and BCR::ABL1-positive acute lymphoblastic leukemia","authors":"Jitka Krizkova, Vaclava Polivkova, Adam Laznicka, Nikola Curik, Adela Benesova, Pavla Suchankova, Tomas Smazik, Veronika Vysinova, Dana Mikulenkova, Hana Klamova, Marketa Stastna Markova, Dana Srbova, Jan Zuna, Marketa Zaliova, Jan Trka, Cyril Salek, Katerina Machova Polakova","doi":"10.1038/s41375-025-02609-3","DOIUrl":"https://doi.org/10.1038/s41375-025-02609-3","url":null,"abstract":"<p>Adolescent and young adults (AYAs) with chronic myeloid leukemia in chronic phase (CML-CP) reportedly respond worse to tyrosine kinase inhibitors (TKIs) than adults, potentially due to additional genetic abnormalities, including mutations in cancer-related genes (CRGs). This real-life study compared mutation profiles and their impact on outcomes in 80 AYA, 97 adult, and 16 pediatric CML-CP patients, alongside 81 <i>BCR::ABL1</i>-positive acute lymphoblastic leukemia (Ph+ ALL) patients. CRG mutations were more frequent in AYAs (25.0%) than in adults (19.6%) or children (12.5%). AYAs with Ph+ ALL exhibited higher mutational frequencies (53.3%) compared to children (26.7%) and adults (38.9%). At diagnosis, mutations in <i>ASXL1</i>, <i>DNMT3A</i>, and <i>TET2</i> dominated in CML-CP and <i>RUNX1</i>, <i>IKZF1</i>, and <i>BCR::ABL1</i> in Ph+ ALL. <i>ASXL1</i> mutations correlated with reduced progression-free survival (PFS) in AYAs and adults. Unlike adults, AYAs showed no increase in <i>BCR::ABL1</i> kinase domain mutations during TKI therapy. Nilotinib improved PFS in AYAs with <i>ASXL1</i> mutations, highlighting the efficacy of higher-generation TKIs. <i>ASXL1</i> mutations also impaired erythropoiesis, warranting further validation. Despite a higher mutational burden, AYAs did not exhibit worse prognoses than adults. Lower mutation rates at follow-up suggest potential impact of nilotinib. Mutation profiling and optimized TKI use are crucial to mitigate progression risks in CRG-mutated patients.</p><figure></figure>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"77 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143880425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prediction of resistance to hydroxyurea therapy in patients with polycythemia vera: a machine learning study (PV-AIM) validated in a prospective interventional phase IV trial (HU-F-AIM)","authors":"Florian H. Heidel, Valerio De Stefano, Matthias Zaiss, Jens Kisro, Eva Gückel, Susanne Großer, Mike W. Zuurman, Kirsi Manz, Kenneth Bryan, Armita Afsharinejad, Martin Griesshammer, Jean-Jacques Kiladjian","doi":"10.1038/s41375-025-02623-5","DOIUrl":"https://doi.org/10.1038/s41375-025-02623-5","url":null,"abstract":"<p>Polycythemia vera (PV) is a myeloproliferative neoplasm associated with increased thromboembolic (TE) risk and hematologic complications. Hydroxyurea (HU) serves as the most frequently used first-line cytoreductive therapy worldwide; however, resistance to HU (HU-RES) develops in a significant subset of patients, leading to increased morbidity and necessitating alternative treatments. This study, part of the PV-AIM project, employed machine learning techniques on real-world evidence (RWE) from the Optum® EHR database containing 82.960 PV patients to identify baseline predictors of HU-RES within the first 6–9 months of therapy. Using a Random Forest model, the study analyzed data from 1850 patients, focusing on laboratory parameters and clinical characteristics. Key predictive markers included red cell distribution width (RDW) and hemoglobin (HGB), showing the strongest association with HU-RES. A synergistic interaction between RDW and HGB was identified, enabling TE risk stratification. This study provides a robust framework for early detection of HU-RES using readily available clinical data, facilitating timely intervention. These findings underscore the importance of personalized treatment approaches in managing PV and highlight the utility of machine learning in enhancing predictive accuracy and clinical outcomes. Based on the results of PV-AIM we initiated an open-label, prospective, single-arm, interventional, phase IV study (HU-F-AIM) evaluating HU-resistance/intolerance. Validation of predictive biomarkers may facilitate identification of patients at risk of HU resistance who may benefit from alternative treatment options, possibly preventing ongoing phlebotomy during HU treatment, a frequent therapeutic choice in high-risk PV associated with early disease progression and increased thromboembolic complications. We propose an updated terminology that differentiates between true molecular resistance and clinical resistance, that may indicate the requirement for alternative therapeutic strategies.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"1 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143872647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myeloid neoplasms after CD19-directed CAR T cells therapy in long-term B-cell lymphoma responders, a rising risk over time?","authors":"Nicolas Gazeau, David Beauvais, Rémi Tilmont, Micha Srour, Emmanuelle Ferrant, Violaine Safar, Ludovic Fouillet, Pascale Flandrin-Gresta, Nicolas Gower, Paul Chauvet, Nicolas Duployez, Benjamin Podvin, Julie Demaret, Sarah Huet, Pierre Sujobert, Hervé Ghesquières, Gandhi Damaj, Emmanuel Bachy, Franck Morschhauser, Ibrahim Yakoub-Agha, Maël Heiblig, Pierre Sesques","doi":"10.1038/s41375-025-02605-7","DOIUrl":"https://doi.org/10.1038/s41375-025-02605-7","url":null,"abstract":"<p>Therapy-related myeloid neoplasms (t-MN), including myelodysplastic neoplasms (t-MDS) and acute myeloid leukemia (t-AML), have emerged as significant late complications after CAR T cell therapy. We retrospectively analyzed 539 patients with B cell lymphoma treated with CD19 directed CAR T cell therapy across four French centers. Cumulative incidences of t-MN was estimated with relapse or death treated as competing risk. Univariate and propensity score matching (PSM) analyses were conducted to assess risk factors with age and the number of prior treatments as covariates. After a median follow-up of 25 months, the cumulative incidence of t-MN was 4.5% at 2 years. T-MN occurred predominantly as t-MDS (62%) and t-AML (38%) with high cytogenetic risk. Median overall survival after t-MN diagnosis was 4.5 months. In univariate analysis, older age (<i>p </i>&lt; 0.01), higher MCV (<i>p </i>&lt; 0.01), and higher ICANS grade (<i>p </i>= 0.04) were associated with increased risk of t-MN. After PSM, MCV and ICANS grade remained significant risk factors. CAR T cell products with CD28 co-stimulatory domains trended towards higher t-MN risk (<i>p </i>= 0.09). NGS analysis showed that 85.7% of t-MN had pre-existing mutations, most commonly TP53. This study highlights t-MN as a severe late complication of CAR T cell therapy. MCV and ICANS grade were identified as key risk factors.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"2 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143866630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Possible impacts of cosmic radiation on leukemia development during human deep space exploration","authors":"Fay Ghani, Abba C. Zubair","doi":"10.1038/s41375-025-02624-4","DOIUrl":"https://doi.org/10.1038/s41375-025-02624-4","url":null,"abstract":"<p>With the advent of deep space exploration and ambitious plans to return humans to the Moon and journey onward to Mars, humans will face exposure to ionizing radiation beyond Earth’s atmosphere and magnetosphere. This is particularly concerning for the hematopoietic system that is sensitive to galactic cosmic rays (GCRs) during interplanetary missions. Epidemiological studies and animal studies implicate that exposure to ionizing radiation can cause leukemias, with recent consensus showing that almost all types of leukemias, even chronic lymphocytic leukemia, can be caused by ionizing radiation despite previous controversies. The possible deleterious effects of deep space travel on the formation, development, etiology, and pathophysiology of hematologic malignancies, specifically leukemias, remain largely unclear. The mechanism(s) by which ionizing radiations cause leukemia differs for different leukemia types and is poorly understood in the spaceflight environment, posing a serious health risk for future astronauts. This paper provides a comprehensive review of the various studies and evidence available on Earth and in space assessing the relationship between ionizing radiation and increased risk of leukemia. We also discuss the unique characteristics of leukemia in space, ethical considerations, risk assessments and potential challenges this may bring to astronauts and healthcare professionals as humanity continues to explore the cosmos.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"23 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143866631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ATM aberrations in chronic lymphocytic leukemia: del(11q) rather than ATM mutations is an adverse-prognostic biomarker","authors":"Birna Thorvaldsdottir, Larry Mansouri, Lesley-Ann Sutton, Ferran Nadeu, Manja Meggendorfer, Helen Parker, Christian Brieghel, Stamatia Laidou, Riccardo Moia, Davide Rossi, Jana Kotaskova, Julio Delgado, Ana E. Rodríguez-Vicente, Rocío Benito, Gian Matteo Rigolin, Silvia Bonfiglio, Lydia Scarfò, Mattias Mattsson, Zadie Davis, Panagiotis Baliakas, Inmaculada Rapado, Fatima Miras, Joaquín Martinez-Lopez, Javier de la Serna, Jesús María Hernández Rivas, María José Larráyoz, María José Calasanz, Karin E. Smedby, Blanca Espinet, Anna Puiggros, Lars Bullinger, Francesc Bosch, Bárbara Tazón-Vega, Fanny Baran-Marszak, David Oscier, Florence Nguyen-Khac, Thorsten Zenz, Maria Jose Terol, Antonio Cuneo, María Hernández-Sánchez, Sarka Pospisilova, Gianluca Gaidano, Carsten U. Niemann, Elias Campo, Jonathan C. Strefford, Paolo Ghia, Kostas Stamatopoulos, Richard Rosenquist","doi":"10.1038/s41375-025-02615-5","DOIUrl":"https://doi.org/10.1038/s41375-025-02615-5","url":null,"abstract":"<p>Despite the well-established adverse impact of del(11q) in chronic lymphocytic leukemia (CLL), the prognostic significance of somatic <i>ATM</i> mutations remains uncertain. We evaluated the effects of <i>ATM</i> aberrations (del(11q) and/or <i>ATM</i> mutations) on time-to-first-treatment (TTFT) in 3631 untreated patients with CLL, in the context of IGHV gene mutational status and mutations in nine CLL-related genes. <i>ATM</i> mutations were present in 246 cases (6.8%), frequently co-occurring with del(11q) (112/246 cases, 45.5%). <i>ATM</i>-mutated patients displayed a different spectrum of genetic abnormalities when comparing IGHV-mutated (M-CLL) and unmutated (U-CLL) cases: M-CLL was enriched for <i>SF3B1</i> and <i>NFKBIE</i> mutations, whereas U-CLL showed mutual exclusivity with trisomy 12 and <i>TP53</i> mutations. Isolated <i>ATM</i> mutations were rare, affecting 1.2% of Binet A patients and &lt;1% of M-CLL cases. While univariable analysis revealed shorter TTFT for Binet A patients with any <i>ATM</i> aberration compared to <i>ATM</i>-wildtype, multivariable analysis identified only del(11q), trisomy 12, <i>SF3B1</i>, and <i>EGR2</i> mutations as independent prognosticators of shorter TTFT among Binet A patients and within M-CLL and U-CLL subgroups. These findings highlight del(11q), and not <i>ATM</i> mutations, as a key biomarker of increased risk of early progression and need for therapy, particularly in otherwise indolent M-CLL, providing insights into risk-stratification and therapeutic decision-making.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"45 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143866632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-related prognoses of genetic subtypes in B-cell acute lymphoblastic leukemia/lymphoma (B-ALL): insights from a decade of national data","authors":"Ting Zhou, Nicholas J. Short, Nitin Jain, Keyur P. Patel, Elias J. Jabbour, Hagop M. Kantarjian, L. Jeffrey Medeiros, J. Bryan Iorgulescu","doi":"10.1038/s41375-025-02588-5","DOIUrl":"https://doi.org/10.1038/s41375-025-02588-5","url":null,"abstract":"<p>Recurrent chromosomal rearrangements and aneuploidies are founding genetic hallmarks in ~90% of B-lymphoblastic leukemia/lymphoma (B-ALL). Advances in our understanding of B-ALL genetics have transformed the modern classification and management of B-ALL, underscoring the integral role of molecular profiling [1,2,3,4]. Although contemporary risk-directed therapeutic regimens have improved outcomes for patients with B-ALL, not all ages benefit equally. Overall, patient survival rates are inversely correlated with age, from a 5-year overall survival (OS) of &gt;90% in children to &lt;30% in older adults (60+ yr) with standard chemotherapy-based management [5]. The etiology of this age-related decline in B-ALL survival rates remains unclear. Potential explanations include unique underlying distributions of genetic alterations (e.g., with adverse alterations such as <i>BCR</i>::<i>ABL1</i> enriched in older patients, whereas favorable genetic subtypes such as <i>ETV6</i>::<i>RUNX1</i> predominate in younger patients), and worse tolerance of chemotherapy in older adults [6, 7]. We therefore examined the relationships of B-ALL genetic subtype, patient age and outcomes; and whether rare B-ALL genetic subtypes exhibited unique clinicopathologic features.</p><p>Patients diagnosed with B-ALL between 2010 and 2021 were identified from the National Cancer Database (NCDB), which is maintained by the American College of Surgeons and American Cancer Society, and captures &gt;63% of new leukemia diagnoses across the United States from approximately 1,500 Commission on Cancer-accredited academic and community hospitals [8]. The NCDB contains deidentified national data that qualifies for human subjects research exemption. In 2010, cancer registries began collecting data for seven genetically defined B-ALL subtypes introduced in the World Health Organization (WHO) Classification 4th edition (and persist into the 5th edition), as defined by their ICD-O-3 codes: B-ALL with <i>BCR</i>::<i>ABL1</i> (9812/3), <i>ETV6</i>::<i>RUNX1</i> (9814/3), (high) hyperdiploidy (9815/3), <i>KMT2A</i>-rearrangement (9813/3), hypodiploidy (9816/3), <i>TCF3</i>::<i>PBX1</i> (9818/3), and <i>IGH</i>::<i>IL3</i> (9817/3) [1].</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"260 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143866621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}