Pub Date : 2025-11-20DOI: 10.1038/s41375-025-02808-y
David Vallois, Edoardo Missiaglia, Luis Veloza, Anja Fischer, Doriane Cavalieri, Vimel Rattina, Bettina Bisig, Vincent Roh, Laura Wiehle, Rita Sarkis, Emmanuel Bachy, Christophe Bonnet, Julie Bruneau, Anne Cairoli, Roland De Wind, Fanny Drieux, Romain Dubois, Jean-François Emile, Virginie Fataccioli, Kamel Laribi, Albane Ledoux-Pilon, François Lemonnier, Francisco Llamas-Gutierrez, Pierre Morel, Marie Parrens, Elsa Poullot, Leticia Quintanilla-Martinez, Jeremy Sandrini, Joan Somja, Luc Xerri, Olivier Tournilhac, Philippe Gaulard, Reiner Siebert, Laurence de Leval
Pub Date : 2025-11-18DOI: 10.1038/s41375-025-02796-z
Fausto Castagnetti, Massimo Breccia, Elisabetta Abruzzese, Renato Bassan, Gianni Binotto, Massimiliano Bonifacio, Giovanni Caocci, Isabella Capodanno, Francesco Cavazzini, Giuseppe Cimino, Paola Fazi, Antonella Gozzini, Alessandra Iurlo, Jeroen J. W. M. Janssen, Monia Lunghi, Roberto Marasca, Bruno Martino, Monica Messina, Francesco Muriano, Francesca Paoloni, Alfonso Piciocchi, Gianantonio Rosti, Antonella Russo Rossi, Giuseppe Saglio, Simona Sica, Simona Soverini, Agostino Tafuri, Daniele Vallisa, Peter E. Westerweel, Fabrizio Pane
Treatment-free remission is one of the most important goals of CML treatment but so far, the best treatment to reach this aim is still undefined, even though it is widely accepted that a sustained DMR is the prerequisite to discontinue TKI. Here we report on the depth of the molecular response, the first co-primary end point of the SUSTRENIM study, in a cohort of newly diagnosed CP-CML patients randomized 1:1 to be treated with nilotinib or with imatinib followed by switching to nilotinib in absence of optimal response. Of the 448 enrolled patients, 228 and 220 were randomized to the nilotinib (NIL) and imatinib (IM) arms, respectively, and followed for a median of 45.9 months. Eighty-two (37.2%) of the 220 patients on the IMarm did not fulfill the ELN criteria for optimal response of treatment and switched to nilotinib therapy. At the 24 months of follow-up, 107 of the 448 patients reached an MR4.5 response with a significantly higher frequency within the patients on the nilotinib arm (65 vs 42; p = 0.02). The analysis of the first primary endpoint indicates that, despite the early switch in the IM-randomized patients, NIL therapy is more effective to induce DMR.
无治疗缓解是CML治疗最重要的目标之一，但到目前为止，达到这一目标的最佳治疗方法仍然不明确，尽管人们普遍认为持续的DMR是停止TKI的先决条件。在这里，我们报告了分子反应的深度，SUSTRENIM研究的第一个共同主要终点，在一组新诊断的CP-CML患者中，随机1:1地接受尼罗替尼或伊马替尼治疗，然后在没有最佳反应的情况下切换到尼罗替尼。在448名入组患者中，228名和220名分别随机分配到尼罗替尼（NIL）和伊马替尼（IM）组，随访时间中位数为45.9个月。在接受IMarm治疗的220名患者中，有82名（37.2%）未达到ELN治疗最佳反应标准，转而使用尼罗替尼治疗。在24个月的随访中，448例患者中有107例达到MR4.5缓解，尼罗替尼组患者的MR4.5缓解频率显著高于尼罗替尼组（65 vs 42; p = 0.02）。对第一个主要终点的分析表明，尽管在im随机患者中早期切换，但NIL治疗更有效地诱导DMR。
{"title":"Nilotinib versus imatinib with early switch from imatinib to nilotinib to obtain treatment-free remission in newly diagnosed chronic myeloid leukemia patients: the analysis of the first co-primary endpoint","authors":"Fausto Castagnetti, Massimo Breccia, Elisabetta Abruzzese, Renato Bassan, Gianni Binotto, Massimiliano Bonifacio, Giovanni Caocci, Isabella Capodanno, Francesco Cavazzini, Giuseppe Cimino, Paola Fazi, Antonella Gozzini, Alessandra Iurlo, Jeroen J. W. M. Janssen, Monia Lunghi, Roberto Marasca, Bruno Martino, Monica Messina, Francesco Muriano, Francesca Paoloni, Alfonso Piciocchi, Gianantonio Rosti, Antonella Russo Rossi, Giuseppe Saglio, Simona Sica, Simona Soverini, Agostino Tafuri, Daniele Vallisa, Peter E. Westerweel, Fabrizio Pane","doi":"10.1038/s41375-025-02796-z","DOIUrl":"10.1038/s41375-025-02796-z","url":null,"abstract":"Treatment-free remission is one of the most important goals of CML treatment but so far, the best treatment to reach this aim is still undefined, even though it is widely accepted that a sustained DMR is the prerequisite to discontinue TKI. Here we report on the depth of the molecular response, the first co-primary end point of the SUSTRENIM study, in a cohort of newly diagnosed CP-CML patients randomized 1:1 to be treated with nilotinib or with imatinib followed by switching to nilotinib in absence of optimal response. Of the 448 enrolled patients, 228 and 220 were randomized to the nilotinib (NIL) and imatinib (IM) arms, respectively, and followed for a median of 45.9 months. Eighty-two (37.2%) of the 220 patients on the IMarm did not fulfill the ELN criteria for optimal response of treatment and switched to nilotinib therapy. At the 24 months of follow-up, 107 of the 448 patients reached an MR4.5 response with a significantly higher frequency within the patients on the nilotinib arm (65 vs 42; p = 0.02). The analysis of the first primary endpoint indicates that, despite the early switch in the IM-randomized patients, NIL therapy is more effective to induce DMR.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"40 1","pages":"47-54"},"PeriodicalIF":13.4,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41375-025-02796-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145536609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-18DOI: 10.1038/s41375-025-02801-5
Matthew Salmon, Nicole Naumann, Jenny Rinke, Manja Meggendorfer, Deepti Radia, Mark Pomfret, Thomas Ernst, Andreas Hochhaus, Andreas Reiter, William J. Tapper, Helen White, Nicholas C. P. Cross
Diverse haematological neoplasms are driven by tyrosine kinase (TK) fusion genes formed by recurrent or non-recurrent genomic rearrangements. The resulting chimeric proteins often present excellent targets for treatment with kinase inhibitors, and the fusion transcripts or genomic junctions can be used as specific targets for molecular monitoring. Whilst the TK genes involved are generally well characterised (e.g. ABL1, PDGFRA, FGFR1), the fusion partners are very diverse, presenting a challenge for detection and characterisation of these structural variants (SV) using current diagnostic methods. We assessed the ability of targeted nanopore sequencing using adaptive sampling to detect fusion genes in myeloid neoplasms. We sequenced genomic DNA from patients (n = 20) with a known or suspected TK gene fusion and identified rearrangements in 18 cases, including all cases with a known TK fusion, typical and atypical BCR::ABL1 rearrangements, an 843Kb deletion causing a FIP1L1::PDGFRA fusion, novel AGAP2::PDGFRB and NFIA::PDGFRB fusions, and a complex CCDC88C::PDGFRB rearrangement with multiple translocation events. The approach was fast (<72 h/sample from DNA to result), flexible with minimal hands-on laboratory time, and provided accurate, patient-specific characterisation of genomic breakpoints.
{"title":"Long read nanopore DNA sequencing with adaptive sampling to identify tyrosine kinase fusion genes","authors":"Matthew Salmon, Nicole Naumann, Jenny Rinke, Manja Meggendorfer, Deepti Radia, Mark Pomfret, Thomas Ernst, Andreas Hochhaus, Andreas Reiter, William J. Tapper, Helen White, Nicholas C. P. Cross","doi":"10.1038/s41375-025-02801-5","DOIUrl":"10.1038/s41375-025-02801-5","url":null,"abstract":"Diverse haematological neoplasms are driven by tyrosine kinase (TK) fusion genes formed by recurrent or non-recurrent genomic rearrangements. The resulting chimeric proteins often present excellent targets for treatment with kinase inhibitors, and the fusion transcripts or genomic junctions can be used as specific targets for molecular monitoring. Whilst the TK genes involved are generally well characterised (e.g. ABL1, PDGFRA, FGFR1), the fusion partners are very diverse, presenting a challenge for detection and characterisation of these structural variants (SV) using current diagnostic methods. We assessed the ability of targeted nanopore sequencing using adaptive sampling to detect fusion genes in myeloid neoplasms. We sequenced genomic DNA from patients (n = 20) with a known or suspected TK gene fusion and identified rearrangements in 18 cases, including all cases with a known TK fusion, typical and atypical BCR::ABL1 rearrangements, an 843Kb deletion causing a FIP1L1::PDGFRA fusion, novel AGAP2::PDGFRB and NFIA::PDGFRB fusions, and a complex CCDC88C::PDGFRB rearrangement with multiple translocation events. The approach was fast (<72 h/sample from DNA to result), flexible with minimal hands-on laboratory time, and provided accurate, patient-specific characterisation of genomic breakpoints.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"40 1","pages":"37-46"},"PeriodicalIF":13.4,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41375-025-02801-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145536090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-18DOI: 10.1038/s41375-025-02802-4
Maroulio Pertesi, Delphine Demangel, Abhishek Niroula, Emeline Perrial, Maria Laura Mahecha Escobar, Maxime Vallée, Christine Liacos, Mehmet K. Samur, Adam S. Sperling, Nikhil C. Munshi, Efstathios Kastritis, Meletios A. Dimopoulos, James D. McKay, Ulf-Henrik Mellqvist, Markus Hansson, Charles Dumontet, On behalf of the Intergroupe Francophone du Myélome (IFM), Björn Nilsson
Multiple myeloma (MM) is the second most common blood malignancy, with several lines of evidence supporting an inherited genetic component. Here, we sequenced 177 affected individuals from 128 families, and 170 early-onset MM cases diagnosed before 55 years of age. Samples were identified and collected through nationwide efforts in France, Sweden, and Greece. We focused on rare germline protein truncating and likely deleterious missense variants in genes harboring variants in at least two families showing variant-disease segregation, and in additional index (≥2) and/or early-onset (≥2) cases. We identified likely pathogenic variants in ATM (N = 12), ANGPTL6 (N = 5), and FBXW9 (N = 6). Additionally, we detected variants in previously reported MM predisposition genes, including DIS3, EP300, and KDM1A. Our results represent the largest sequencing study on familial and early-onset MM to date, and further illuminate the constitutional genetic basis of MM.
{"title":"Putative multiple myeloma susceptibility genes identified by exome sequencing of 347 familial and early-onset cases","authors":"Maroulio Pertesi, Delphine Demangel, Abhishek Niroula, Emeline Perrial, Maria Laura Mahecha Escobar, Maxime Vallée, Christine Liacos, Mehmet K. Samur, Adam S. Sperling, Nikhil C. Munshi, Efstathios Kastritis, Meletios A. Dimopoulos, James D. McKay, Ulf-Henrik Mellqvist, Markus Hansson, Charles Dumontet, On behalf of the Intergroupe Francophone du Myélome (IFM), Björn Nilsson","doi":"10.1038/s41375-025-02802-4","DOIUrl":"10.1038/s41375-025-02802-4","url":null,"abstract":"Multiple myeloma (MM) is the second most common blood malignancy, with several lines of evidence supporting an inherited genetic component. Here, we sequenced 177 affected individuals from 128 families, and 170 early-onset MM cases diagnosed before 55 years of age. Samples were identified and collected through nationwide efforts in France, Sweden, and Greece. We focused on rare germline protein truncating and likely deleterious missense variants in genes harboring variants in at least two families showing variant-disease segregation, and in additional index (≥2) and/or early-onset (≥2) cases. We identified likely pathogenic variants in ATM (N = 12), ANGPTL6 (N = 5), and FBXW9 (N = 6). Additionally, we detected variants in previously reported MM predisposition genes, including DIS3, EP300, and KDM1A. Our results represent the largest sequencing study on familial and early-onset MM to date, and further illuminate the constitutional genetic basis of MM.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"40 1","pages":"235-240"},"PeriodicalIF":13.4,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145545284","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}
Pub Date : 2025-11-17DOI: 10.1038/s41375-025-02803-3
Pinpin Sui, Ying Li, Juyeong Hong, Caroline R. Delma, Shi Chen, Juan Wang, Peng Zhang, Songmi Han, Asra Noor, Hui Yang, Yakun Pang, Yu Luan, Mingjiang Xu, Jihoon Lee, Feng-Chun Yang
Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by high incidence, poor prognosis, and marked genetic and clinical heterogeneity. This heterogeneity poses a significant challenge to effective treatment and underscores the urgent need for tailored therapeutic strategies. Here, we identified the EvC ciliary complex subunits EVC and EVC2 as aberrantly overexpressed in a subset of AMLs, particularly those harboring ASXL1 mutations or the t(8;21) translocation, with elevated expression correlating with poor patient prognosis. Functional studies demonstrated that EVC/EVC2 are essential for maintaining the leukemogenic properties of AML cells, while being dispensable for the function of normal hematopoietic stem/progenitor cells. Loss of EVC/EVC2 impairs leukemia cell proliferation, promotes differentiation, and effectively blocks AML progression in vivo. Mechanistically, we revealed that elevated EVC/EVC2 expression is associated with gained AML1-ETO occupancy or enhanced chromatin interactions at EVC/EVC2 promoter regions in AML cells carrying t(8;21) or ASXL1 mutations, respectively. Notably, we demonstrate that the leukemogenic role of EVC/EVC2 is mediated through MYC pathway activation, independent of their canonical role in Hedgehog signaling. Collectively, our findings demonstrate an oncogenic event of overexpressed EVC/EVC2, identifying novel therapeutic vulnerabilities in AML.
{"title":"Oncogenic activation of EVC/EVC2 defines a therapeutically targetable subset of acute myeloid leukemia","authors":"Pinpin Sui, Ying Li, Juyeong Hong, Caroline R. Delma, Shi Chen, Juan Wang, Peng Zhang, Songmi Han, Asra Noor, Hui Yang, Yakun Pang, Yu Luan, Mingjiang Xu, Jihoon Lee, Feng-Chun Yang","doi":"10.1038/s41375-025-02803-3","DOIUrl":"10.1038/s41375-025-02803-3","url":null,"abstract":"Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by high incidence, poor prognosis, and marked genetic and clinical heterogeneity. This heterogeneity poses a significant challenge to effective treatment and underscores the urgent need for tailored therapeutic strategies. Here, we identified the EvC ciliary complex subunits EVC and EVC2 as aberrantly overexpressed in a subset of AMLs, particularly those harboring ASXL1 mutations or the t(8;21) translocation, with elevated expression correlating with poor patient prognosis. Functional studies demonstrated that EVC/EVC2 are essential for maintaining the leukemogenic properties of AML cells, while being dispensable for the function of normal hematopoietic stem/progenitor cells. Loss of EVC/EVC2 impairs leukemia cell proliferation, promotes differentiation, and effectively blocks AML progression in vivo. Mechanistically, we revealed that elevated EVC/EVC2 expression is associated with gained AML1-ETO occupancy or enhanced chromatin interactions at EVC/EVC2 promoter regions in AML cells carrying t(8;21) or ASXL1 mutations, respectively. Notably, we demonstrate that the leukemogenic role of EVC/EVC2 is mediated through MYC pathway activation, independent of their canonical role in Hedgehog signaling. Collectively, our findings demonstrate an oncogenic event of overexpressed EVC/EVC2, identifying novel therapeutic vulnerabilities in AML.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"40 1","pages":"166-177"},"PeriodicalIF":13.4,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145531658","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}
Pub Date : 2025-11-17DOI: 10.1038/s41375-025-02805-1
Florian H. Heidel, Martin Griesshammer, Jean-Jacques Kiladjian, on behalf of the PV-AIM investigators
{"title":"Response to the commentary by Xu et al. on the PV-AIM study","authors":"Florian H. Heidel, Martin Griesshammer, Jean-Jacques Kiladjian, on behalf of the PV-AIM investigators","doi":"10.1038/s41375-025-02805-1","DOIUrl":"10.1038/s41375-025-02805-1","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"40 1","pages":"247-249"},"PeriodicalIF":13.4,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41375-025-02805-1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145541183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-12DOI: 10.1038/s41375-025-02812-2
Hanxue Zheng, Liansheng Zhang, Lijuan Li
{"title":"Correspondence to “Regulation of metabolic adaptation and leukemia progression by MUSASHI2-DEPTOR-KIF11 axis”","authors":"Hanxue Zheng, Liansheng Zhang, Lijuan Li","doi":"10.1038/s41375-025-02812-2","DOIUrl":"10.1038/s41375-025-02812-2","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"40 1","pages":"245-246"},"PeriodicalIF":13.4,"publicationDate":"2025-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145492573","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}
Pub Date : 2025-11-12DOI: 10.1038/s41375-025-02809-x
Wei Wei, Zhihui Song, Yajun Wang, Shen Li, Lingli Tan, John Lee, Kathy Q. Cai, Reza Nejati, Marshall E. Kadin, Kerry S. Campbell, Masao Nakagawa, Yibin Yang
Anaplastic large cell lymphoma (ALCL), an aggressive T-cell malignancy, is marked by elevated expression of CD30 and the immune checkpoint molecule PD-L1. While CD30-directed chimeric antigen receptor (CAR) therapies have demonstrated clinical promise, therapeutic resistance remains a major hurdle. Here, we conducted integrated genome-wide CRISPR-Cas9 loss-of-function screens using CD30-specific CAR-engineered natural killer (CAR-NK) cells, alongside a complementary PD-L1 regulator screen, and uncovered a critical role for interleukin-1 receptor (IL-1R) signaling in modulating CAR therapy efficacy in both ALK⁺ and ALK⁻ ALCL. Mechanistically, IL-1R signaling drives an NFKBIZ – IL-17F – MAPK axis that sustains PD-L1 expression via an autocrine loop, while simultaneously inducing proinflammatory cytokines and chemokines that reinforce immune evasion and shape an immunosuppressive tumor microenvironment. Notably, NFKBIZ (IκBζ) emerges as a central transcriptional regulator orchestrating this immune suppression program upstream of IL-17F. Importantly, pharmacologic inhibition of IL-1R signaling significantly enhances the antitumor activity of CD30-specific CAR therapies both in vitro and in ALCL xenograft models. Collectively, our findings uncover a novel mechanism of immune resistance and nominate IL-1R blockade as a promising combinatorial strategy to improve CAR-based immunotherapy in ALCL.
{"title":"The IL-1R and NFKBIZ pathway mediates immunoregulatory responses and immunotherapy efficacy in anaplastic large cell lymphoma","authors":"Wei Wei, Zhihui Song, Yajun Wang, Shen Li, Lingli Tan, John Lee, Kathy Q. Cai, Reza Nejati, Marshall E. Kadin, Kerry S. Campbell, Masao Nakagawa, Yibin Yang","doi":"10.1038/s41375-025-02809-x","DOIUrl":"10.1038/s41375-025-02809-x","url":null,"abstract":"Anaplastic large cell lymphoma (ALCL), an aggressive T-cell malignancy, is marked by elevated expression of CD30 and the immune checkpoint molecule PD-L1. While CD30-directed chimeric antigen receptor (CAR) therapies have demonstrated clinical promise, therapeutic resistance remains a major hurdle. Here, we conducted integrated genome-wide CRISPR-Cas9 loss-of-function screens using CD30-specific CAR-engineered natural killer (CAR-NK) cells, alongside a complementary PD-L1 regulator screen, and uncovered a critical role for interleukin-1 receptor (IL-1R) signaling in modulating CAR therapy efficacy in both ALK⁺ and ALK⁻ ALCL. Mechanistically, IL-1R signaling drives an NFKBIZ – IL-17F – MAPK axis that sustains PD-L1 expression via an autocrine loop, while simultaneously inducing proinflammatory cytokines and chemokines that reinforce immune evasion and shape an immunosuppressive tumor microenvironment. Notably, NFKBIZ (IκBζ) emerges as a central transcriptional regulator orchestrating this immune suppression program upstream of IL-17F. Importantly, pharmacologic inhibition of IL-1R signaling significantly enhances the antitumor activity of CD30-specific CAR therapies both in vitro and in ALCL xenograft models. Collectively, our findings uncover a novel mechanism of immune resistance and nominate IL-1R blockade as a promising combinatorial strategy to improve CAR-based immunotherapy in ALCL.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"40 1","pages":"152-165"},"PeriodicalIF":13.4,"publicationDate":"2025-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145492524","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：