LeukemiaPub Date : 2026-10-19DOI: 10.1038/s41375-026-03177-w
Giovanni Barosi, Vittorio Rosti, Annalisa De Silvestri, Robert Peter Gale
{"title":"Predicting long-term survival in primary myelofibrosis","authors":"Giovanni Barosi, Vittorio Rosti, Annalisa De Silvestri, Robert Peter Gale","doi":"10.1038/s41375-026-03177-w","DOIUrl":"https://doi.org/10.1038/s41375-026-03177-w","url":null,"abstract":"We interrogated data from 217 subjects with primary myelofibrosis (PMF) diagnosed before 2001 to identify covariates at diagnosis associated with long-term survival. Forty-one survived more than 25 years. Long-term survivors were more often female, younger than 50 years and less likely to have anemia, splenomegaly, increased blood CD34-positive cells, a JAK2V617F variant, and more likely to have grade-0 bone marrow fibrosis and increased platelets. In multivariable logistic regression analyses, age <50 years, platelet count >450 × 10⁹/L, and grade-0 bone marrow fibrosis independently predicted long-term survival. These co-variate associations were confirmed in Cox regression with landmark analyses. Long-term survivors had a lower cumulative incidence of anemia and thrombocytopenia during follow-up. Identifying long-term survivors at diagnosis provides clinically meaningful prognostic information in PMF and may influence therapy decisions.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"32 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149218132","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":"Targeting the mitochondrial complex I subunit NDUFS2 potentiates FLT3 inhibition in acute myeloid leukaemia with FLT3 internal tandem duplication","authors":"Xiqin Tong, Guopeng Chen, Yuzhe Pan, Yanling Chen, Yuxin Tan, Hongqiang Jiang, Qian Wang, Linlu Ma, Ruihang Li, Yuxing Liang, Xiaoyan Liu, Fuling Zhou","doi":"10.1038/s41375-026-03170-3","DOIUrl":"https://doi.org/10.1038/s41375-026-03170-3","url":null,"abstract":"Acute myeloid leukaemia (AML) with FLT3 internal tandem duplication (FLT3-ITD) frequently relapses after FLT3 tyrosine kinase inhibitor (TKI) therapy, highlighting the need to define mechanisms of drug tolerance. Here, we identify the mitochondrial complex I core subunit NDUFS2 as a determinant of FLT3 TKI tolerance in FLT3-ITD AML. A metabolism-focused CRISPR-Cas9 sensitiser screen, integrated with transcriptomic profiling of gilteritinib-resistant cells and primary samples, identified NDUFS2 as upregulated in acquired resistance and preferentially expressed in FLT3-ITD AML. NDUFS2 knockdown impaired complex I activity, oxidative phosphorylation, mitochondrial membrane potential and ATP production, thereby promoting apoptosis and sensitising FLT3-ITD AML cells to gilteritinib. Pharmacologic complex I inhibition with IACS-010759 similarly enhanced gilteritinib activity in FLT3-ITD AML cell lines and primary FLT3-ITD samples, activated AMPK-PERK-ATF4-CHOP stress signalling, promoted apoptosis, and reduced leukaemia burden in a patient-derived xenograft model. Genetic NDUFS2 knockdown also prolonged survival in a xenograft model. A preliminary murine safety assessment showed no overt toxicity under the tested short-term dosing schedule. These findings identify NDUFS2-dependent complex I activity as an adaptive metabolic dependency supporting FLT3 inhibitor tolerance and provide mechanistic insight for further preclinical evaluation.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"11 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149218136","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}
LeukemiaPub Date : 2026-10-16DOI: 10.1038/s41375-026-03167-y
Andrea Visentin, Enrico Gaffo, Moritz Fürstenau, Kerry A Rogers, Baliakas Panagiotis, Chenghua Cui, Cecelia Miller, Claudia Haferlach, Karla Plevova, David Oscier, Zadie Davis, Florence Nguyen-Khac, Eleonora Roncaglia, Gian Matteo Rigolin, Anastasia Athanasiadou, Fanny Baran-Marszak, Alberto Valiente, Maria José Terol, Pau Abrisqueta, Blanca Espinet, Anna Puiggros, Annalisa Martines, Laura Bonaldi, Francesca Romana Mauro, Lydia Scarfò, Thomas Chatzikonstantinou, Eugen Tausch, Karl-Anton Kreuzer, Arnon P Kater, Francesc Bosch, Michael Doubek, Panagiotis Panagiotidis, Olga Kalashnikova, Federica Frezzato, Giulia Calabretto, Valeria Ruocco, Silvia Orsi, Alessandro Cellini, Francesco Angotzi, Andrea Serafin, Shuhua Yi, Barbara Eichhorst, Jennifer A Woyach, Antonio Cuneo, Paolo Ghia, Kostas Stamatopoulos, Livio Trentin, Stefania Bortoluzzi
{"title":"Correction: Clinical and transcriptomic characterization of patients with chronic lymphocytic leukemia harboring t(14;19): an ERIC study.","authors":"Andrea Visentin, Enrico Gaffo, Moritz Fürstenau, Kerry A Rogers, Baliakas Panagiotis, Chenghua Cui, Cecelia Miller, Claudia Haferlach, Karla Plevova, David Oscier, Zadie Davis, Florence Nguyen-Khac, Eleonora Roncaglia, Gian Matteo Rigolin, Anastasia Athanasiadou, Fanny Baran-Marszak, Alberto Valiente, Maria José Terol, Pau Abrisqueta, Blanca Espinet, Anna Puiggros, Annalisa Martines, Laura Bonaldi, Francesca Romana Mauro, Lydia Scarfò, Thomas Chatzikonstantinou, Eugen Tausch, Karl-Anton Kreuzer, Arnon P Kater, Francesc Bosch, Michael Doubek, Panagiotis Panagiotidis, Olga Kalashnikova, Federica Frezzato, Giulia Calabretto, Valeria Ruocco, Silvia Orsi, Alessandro Cellini, Francesco Angotzi, Andrea Serafin, Shuhua Yi, Barbara Eichhorst, Jennifer A Woyach, Antonio Cuneo, Paolo Ghia, Kostas Stamatopoulos, Livio Trentin, Stefania Bortoluzzi","doi":"10.1038/s41375-026-03167-y","DOIUrl":"https://doi.org/10.1038/s41375-026-03167-y","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":" ","pages":""},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149207240","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}
LeukemiaPub Date : 2026-10-16DOI: 10.1038/s41375-026-03157-0
Ryan Yen, Andrew Wu, Min Chen, Lambert Yue, Michael M Lizardo, Christopher S Hughes, Josephine Leung, Yingying Liu, Donna L Forrest, Poul H Sorensen, Steven Pelech, Xiaoyan Jiang
{"title":"Targeting the eIF4F translation initiation complex disrupts BCR::ABL1 translation and overcomes drug resistance in CML.","authors":"Ryan Yen, Andrew Wu, Min Chen, Lambert Yue, Michael M Lizardo, Christopher S Hughes, Josephine Leung, Yingying Liu, Donna L Forrest, Poul H Sorensen, Steven Pelech, Xiaoyan Jiang","doi":"10.1038/s41375-026-03157-0","DOIUrl":"https://doi.org/10.1038/s41375-026-03157-0","url":null,"abstract":"<p><p>Chronic myeloid leukemia (CML) is driven by the constitutively active BCR::ABL1 kinase, which promotes uncontrolled cell proliferation. Although protein-tyrosine kinase inhibitors (TKIs) have revolutionized CML treatment, resistance remains a significant barrier to curative therapy, particularly due to BCR::ABL1 mutations and the persistence of leukemia stem cells (LSCs). New treatment strategies that directly inhibit BCR::ABL1 protein expression are needed to achieve more effective therapy. Using a high-content antibody microarray and bioinformatics analyses, we investigated differences in the proteome and phosphorylation landscape of Imatinib (IM)-resistant cells and identified highly activated members of the eukaryotic translation initiation complex (eIF4F), particularly eIF4G1, a core component of eIF4F. These eIF4F complex members are highly expressed and activated in CD34<sup>+</sup> CML stem/progenitor cells and in IM-resistant cells. Genetic inhibition of eIF4G1 or pharmacological targeting with the small-molecule inhibitor SBI-756 diminished eIF4F complex assembly, reduced overall translation initiation, reduced BCR::ABL1 expression and key downstream targets, impaired the survival of nonresponder stem/progenitor cells, including BCR::ABL1-T315I mutant cells, and sensitized them to TKIs, with strong synergistic effects in vitro and in a PDX model. These findings underscore the potential of eIF4F complex inhibition as a new therapeutic strategy to overcome TKI resistance in CML and other BCR::ABL1<sup>+</sup> malignancies.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":" ","pages":""},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149207230","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}
LeukemiaPub Date : 2026-10-14DOI: 10.1038/s41375-026-03169-w
Shengchun Wang, Shilpa Rao, Cosimo Lobello, David Rushmore, Bhaumik Shah, Suzanne Paley, Pradeep Gupta, Andrew Kalgren, Dinesh Singh, Neil V Sen, Katrin Kurz, Phassawan Rungsiprakarn, Nashwa Mansoor, Brigitte Dade, Ashishkumar Sonani, Vanessa Dupoux, K Qi Cai, Nicholas Mackrides, Donald Baldwin, Peter D Karp, Mowafaq Jillab, German Ott, Reza Nejati, Kavindra Nath, Johnvesly Basappa, Mariusz A Wasik
{"title":"Neoantigenic receptor ROR1 promotes cell growth through diverse and complementary mechanisms.","authors":"Shengchun Wang, Shilpa Rao, Cosimo Lobello, David Rushmore, Bhaumik Shah, Suzanne Paley, Pradeep Gupta, Andrew Kalgren, Dinesh Singh, Neil V Sen, Katrin Kurz, Phassawan Rungsiprakarn, Nashwa Mansoor, Brigitte Dade, Ashishkumar Sonani, Vanessa Dupoux, K Qi Cai, Nicholas Mackrides, Donald Baldwin, Peter D Karp, Mowafaq Jillab, German Ott, Reza Nejati, Kavindra Nath, Johnvesly Basappa, Mariusz A Wasik","doi":"10.1038/s41375-026-03169-w","DOIUrl":"10.1038/s41375-026-03169-w","url":null,"abstract":"<p><p>Aberrant expression of neoantigenic receptor ROR1 has been identified in diverse lymphomas, including mantle cell lymphoma (MCL) and in a broad spectrum of nonlymphoid malignancies. While ROR1 has emerged as an attractive therapeutic target, its oncogenic role and the underlying mechanisms remain rather poorly characterized. Focusing on MCL, we found that ROR1 expression is heterogeneous and it can be induced under environmental stress. Inhibition of ROR1 expression resulted in cell-cycle suppression and apoptotic cell death. The ROR1 loss affected expression of numerous genes and altered phosphorylation of many proteins, including those involved in cell-cycle progression. ROR1 also promotes the synthesis of pyrimidines and purines, including induction of phosphorylation of enzymes involved in pyrimidine synthesis. Finally, we found that ROR1 induced phosphorylation of DEK and that its depletion abrogates ROR1 expression. These results provide insights into the multi-faceted oncogenic role of ROR1, further justifying targeting ROR1 in MCL and other malignancies.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":" ","pages":""},"PeriodicalIF":8.8,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149182843","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}
LeukemiaPub Date : 2026-10-13DOI: 10.1038/s41375-026-03143-6
Matthew A Timmins, Jingyu Chen, Andrew Moore, Sophie Kogut, Hana Paculova, Seth Frietze, Ingo Ringshausen
{"title":"Fibroblast growth factor receptor-signaling confers stroma-mediated drug resistance in malignant B cells.","authors":"Matthew A Timmins, Jingyu Chen, Andrew Moore, Sophie Kogut, Hana Paculova, Seth Frietze, Ingo Ringshausen","doi":"10.1038/s41375-026-03143-6","DOIUrl":"https://doi.org/10.1038/s41375-026-03143-6","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":" ","pages":""},"PeriodicalIF":8.8,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149182730","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}
LeukemiaPub Date : 2026-10-13DOI: 10.1038/s41375-026-03160-5
Romain Vazquez, Maxime Sajot, Jad Nasrallah, Rudy Birsen, Ismaël Boussaid, Morgane Plevenage, Zubaidan Tuerdi, Axelle Guedon, Lilia Cantero Aguilar, Tony Huynh, Natacha Johnson, Chloé Friedrich, Eric Grignano, Justine Decroocq, Lise Willems, Carole Almire, Marie-Clotilde Alves-Guerra, Evelyne Lauret, Yannick Simoni, Michaela Fontenay, Olivier Kosmider, Didier Bouscary, Clement Larrue, Nicolas Chapuis
{"title":"Inhibition of PHB2/PINK1-mediated mitophagy potentiates venetoclax activity in acute myeloid leukemia.","authors":"Romain Vazquez, Maxime Sajot, Jad Nasrallah, Rudy Birsen, Ismaël Boussaid, Morgane Plevenage, Zubaidan Tuerdi, Axelle Guedon, Lilia Cantero Aguilar, Tony Huynh, Natacha Johnson, Chloé Friedrich, Eric Grignano, Justine Decroocq, Lise Willems, Carole Almire, Marie-Clotilde Alves-Guerra, Evelyne Lauret, Yannick Simoni, Michaela Fontenay, Olivier Kosmider, Didier Bouscary, Clement Larrue, Nicolas Chapuis","doi":"10.1038/s41375-026-03160-5","DOIUrl":"https://doi.org/10.1038/s41375-026-03160-5","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) cells are highly dependent on mitochondrial activity for survival, with this metabolic reliance driven in part by BCL-2, which is therapeutically targeted by venetoclax-based therapies. The regulation of mitochondrial dynamics in leukemic cells is therefore essential for maintaining mitochondrial homeostasis. However, the mechanisms that enable selective degradation of damaged mitochondria (mitophagy) are still poorly understood in AML. In this study, we sought to elucidate the role of PTEN-induced putative kinase 1 (PINK1), a key sensor of mitochondrial stress, in regulating mitophagy in leukemic cells. Our results identified PINK1 as a central modulator of mitophagy. Genetic depletion of PINK1 reduced both basal and stress-induced mitophagy, leading to mitochondria accumulation and functional impairment. Additionally, we discovered that PINK1 stabilization during mitochondrial stress is regulated by Prohibitin 2 (PHB2), and that depletion or inhibition of PHB2 mirrored the biological effects of PINK1 loss. Notably, both genetic depletion of PINK1 or PHB2, as well as pharmacological inhibition of PHB2, significantly increased AML cell sensitivity to venetoclax both in vitro and in vivo. Together, these findings highlight the potential of targeting the PHB2/PINK1 signalling pathway to improve the efficacy of venetoclax-based therapies in AML by disrupting the mitophagy process.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":" ","pages":""},"PeriodicalIF":8.8,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149182880","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}
LeukemiaPub Date : 2026-10-12DOI: 10.1038/s41375-026-03159-y
Qing Yin, Jing Gao, Xiangao Huang, Allen Hu, Rui Xiong, Jeffrey W Craig, Kevin Qiu, Loryn Blackburn, Amy S Schienschang, Sarah A Whitaker, Archana Thakur, Craig A Portell, Daniel W Lee, Shane Wei, Lawrence G Lum, Selina Chen-Kiang, Michael E Williams, Jianguo Tao
{"title":"Combating CD24 to overcome CD19 CAR-T resistance via induction of innate and adaptive immunity in B-cell malignancies.","authors":"Qing Yin, Jing Gao, Xiangao Huang, Allen Hu, Rui Xiong, Jeffrey W Craig, Kevin Qiu, Loryn Blackburn, Amy S Schienschang, Sarah A Whitaker, Archana Thakur, Craig A Portell, Daniel W Lee, Shane Wei, Lawrence G Lum, Selina Chen-Kiang, Michael E Williams, Jianguo Tao","doi":"10.1038/s41375-026-03159-y","DOIUrl":"https://doi.org/10.1038/s41375-026-03159-y","url":null,"abstract":"<p><p>CD24 is highly expressed in aggressive B-cell malignancies and represents a novel immunologic vulnerability to overcome resistance to CD19 chimeric antigen receptor T-cell (CAR-T) therapy. We developed a CD24 × CD3 bispecific antibody (CD24 BsAb) and CXCR3-armed CD24 CAR-T cells, both exhibiting potent antitumor activity in lymphoma and leukemia models. CD24 BsAb and CD24 CAR-T overcome CD19 CAR-T resistance driven by antigen loss and apoptosis defects in vitro and in vivo. Beyond direct cytotoxicity, CD24-targeted T cells reprogram macrophages toward an M1-like phenotype and enhance phagocytic clearance. We further engineered a dual-specific, dual-functional CD19 CAR-T that secretes a CD24 bispecific T-cell engager (CD24 BiTE), enabling simultaneous targeting of CD19 and CD24 to address tumor heterogeneity and achieve superior efficacy. Collectively, our study demonstrates that CD24-directed adoptive T-cell therapies are warranted for B-cell malignancies through robust induction of both innate and adaptive immune responses.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":" ","pages":""},"PeriodicalIF":8.8,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166472","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}
LeukemiaPub Date : 2026-10-12DOI: 10.1038/s41375-026-03151-6
Katie Erdos, Madhu M Ouseph, Spencer Krichevsky, Julia T Geyer, Neville Lee, Richard T Silver, Rajarsi Gupta, Ghaith Abu-Zeinah, Joseph M Scandura
{"title":"Marrow hypercellularity is common and clinically neutral in essential thrombocythemia.","authors":"Katie Erdos, Madhu M Ouseph, Spencer Krichevsky, Julia T Geyer, Neville Lee, Richard T Silver, Rajarsi Gupta, Ghaith Abu-Zeinah, Joseph M Scandura","doi":"10.1038/s41375-026-03151-6","DOIUrl":"https://doi.org/10.1038/s41375-026-03151-6","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":" ","pages":""},"PeriodicalIF":8.8,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149170086","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}
LeukemiaPub Date : 2026-10-12DOI: 10.1038/s41375-026-03171-2
Marina Mitrou, Li Li, Bao Ho Nguyen, Gi-Jun Sung, Ky-Youb Nam, Kyu-Tae Kim, Jeong-Hyeok Yoon, Michelle Wang, David Young, Ruiqi Zhu, Tessa Seale, Seung-Hye Choi, Taebo Sim, Donald Small
{"title":"PHI-101: a novel FLT3 inhibitor with potent activity against the F691L gatekeeper resistance mutation.","authors":"Marina Mitrou, Li Li, Bao Ho Nguyen, Gi-Jun Sung, Ky-Youb Nam, Kyu-Tae Kim, Jeong-Hyeok Yoon, Michelle Wang, David Young, Ruiqi Zhu, Tessa Seale, Seung-Hye Choi, Taebo Sim, Donald Small","doi":"10.1038/s41375-026-03171-2","DOIUrl":"https://doi.org/10.1038/s41375-026-03171-2","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":" ","pages":""},"PeriodicalIF":8.8,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149167206","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}
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