IF 13.4 1区医学

Leukemia Pub Date : 2025-10-17 DOI: 10.1038/s41375-025-02788-z

Thi Thanh Vu, Friedrich Stölzel, Kristy W Wang, Christoph Röllig, Melinda L Tursky, Timothy J Molloy, David D Ma

引用次数: 0

DNA methylation alterations in acute lymphoblastic leukemia survivors with late neurocognitive deficits. 晚期神经认知缺陷急性淋巴细胞白血病幸存者的DNA甲基化改变。

IF 11.4 1区医学

Leukemia Pub Date : 2025-10-17 DOI: 10.1038/s41375-025-02779-0

Sarah J Goodman,Darci T Butcher,Sharon L Guger,Eric Diehl,Jack Brzezinski,Brenda Spiegler,Brian J Nieman,Prajkta Kallurkar,Aubrée Boulet Craig,Maja Krajinovic,Julie Laniel,Caroline Laverdière,Daniel Sinnett,Sarah Lippé,Andrei Turinsky,Mary Shago,Lisa J Strug,Shinya Ito,Johann K Hitzler,Russell Schachar,Rosanna Weksberg

引用次数: 0

OGG1 activation improves T cell resilience to oxidative stress after allo-SCT and T cell engager exposure. 激活OGG1可改善同种异体sct和T细胞接合物暴露后T细胞对氧化应激的恢复能力。

IF 11.4 1区医学

Leukemia Pub Date : 2025-10-15 DOI: 10.1038/s41375-025-02783-4

D Saul,C Lischer,H Bruns,N Ziegler,A Kannt,M Michel,D Mougiakakos

引用次数: 0

Defining remission following hematopoietic cell transplant for myelofibrosis: an international expert panel consensus. 定义骨髓纤维化的造血细胞移植后缓解：国际专家小组共识。

IF 11.4 1区医学

Leukemia Pub Date : 2025-10-13 DOI: 10.1038/s41375-025-02754-9

Rachel B Salit,Elizabeth O Hexner,Nico Gagelmann,Nicolaus Kröger,Donal P McLornan,Tania Jain,Vikas Gupta,Gabriela S Hobbs,Roni Tamari,Marie Robin,Bart Scott,Wael Saber

引用次数: 0

Does everyone with newly-diagnosed, untreated acute myeloid leukaemia need remission-induction chemotherapy before advancing to a transplant? 是否每个新诊断的未经治疗的急性髓性白血病患者在进行移植前都需要缓解诱导化疗？

IF 11.4 1区医学

Leukemia Pub Date : 2025-10-13 DOI: 10.1038/s41375-025-02784-3

E Rodríguez-Arbolí,R P Gale

引用次数: 0

Publisher Correction: Suppression of Rho-associated kinase 1 (ROCK1) promotes human hematopoietic stem cell expansion by attenuating mitochondrial fission. 发布者更正：抑制rho相关激酶1 （ROCK1）通过减弱线粒体裂变促进人类造血干细胞扩增。

IF 13.4 1区医学

Leukemia Pub Date : 2025-10-13 DOI: 10.1038/s41375-025-02786-1

Xuepeng Wang, Baskar Ramdas, Ramesh Kumar, Ji Zhang, Reuben Kapur

引用次数: 0

Heart failure in patients with acute myeloid leukemia (AML) treated with anthracycline agents during remission induction therapy: a systematic review and meta-analysis. 急性髓系白血病（AML）患者在缓解诱导治疗期间接受蒽环类药物治疗的心力衰竭：一项系统回顾和荟萃分析。

IF 11.4 1区医学

Leukemia Pub Date : 2025-10-10 DOI: 10.1038/s41375-025-02753-w

Jesse Geels,Anna van Rhenen,Patrycja Gradowska,Folkert W Asselbergs,Marijke Linschoten

{"title":"Heart failure in patients with acute myeloid leukemia (AML) treated with anthracycline agents during remission induction therapy: a systematic review and meta-analysis.","authors":"Jesse Geels,Anna van Rhenen,Patrycja Gradowska,Folkert W Asselbergs,Marijke Linschoten","doi":"10.1038/s41375-025-02753-w","DOIUrl":"https://doi.org/10.1038/s41375-025-02753-w","url":null,"abstract":"Patients with acute myeloid leukemia (AML) are at increased risk of cardiovascular disease, particularly heart failure. Anthracyclines are integral to remission induction therapy in patients eligible for intensive treatment and well-known for their association with cardiotoxicity. However, the incidence of heart failure and other cardiovascular adverse events (CVAEs), as well as differences across various anthracycline agents, has not been comprehensively assessed. We systematically searched PubMed and EMBASE for studies conducted in AML patients treated with anthracyclines during remission induction. Forty-one studies (5995 patients), primarily clinical trials, published between February 1991 and March 2024 were included. The pooled proportion of heart failure was 3.2% (95% CI 1.0-6.2) overall and 2.3% (95% CI 1.4-3.3), 5.0% (95% CI 0.3-14.1) and 10.2% (95% CI 2.4-21.7) for patients treated with daunorubicin, idarubicin or mitoxantrone respectively. Cardiac function was infrequently monitored, and CVAE reporting was generally poor. Since current adverse event grading systems primarily rely on clinical symptoms to assign severity, significant asymptomatic declines in cardiac function will remain undetected. Enhanced CVAE monitoring and reporting, along with revisions to established grading systems, is needed to better identify subclinical cardiotoxicity in AML patients, enabling timely intervention to prevent progression to more advanced heart failure stages.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"2 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145261390","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}

引用次数: 0

Distinct characteristics of VEXAS-causative UBA1 M41 and recurrent functional non-M41 mutations. 引起vexas的UBA1 M41和复发性功能性非M41突变的独特特征。

IF 11.4 1区医学

Leukemia Pub Date : 2025-10-09 DOI: 10.1038/s41375-025-02775-4

Maki Sakuma,Amy K Wang,Samuel J Magaziner,Sachiko P Keane,Manja Meggendorfer,Wolfgang Kern,Claudia Haferlach,Torsten Haferlach,David B Beck,Wencke Walter

{"title":"Distinct characteristics of VEXAS-causative UBA1 M41 and recurrent functional non-M41 mutations.","authors":"Maki Sakuma,Amy K Wang,Samuel J Magaziner,Sachiko P Keane,Manja Meggendorfer,Wolfgang Kern,Claudia Haferlach,Torsten Haferlach,David B Beck,Wencke Walter","doi":"10.1038/s41375-025-02775-4","DOIUrl":"https://doi.org/10.1038/s41375-025-02775-4","url":null,"abstract":"VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is a severe inflammatory and hematologic disease caused by somatic mutations in UBA1. Canonical pathogenic mutations at UBA1 p.Met41 (M41) lead to the loss of the cytoplasmic isoform (UBA1b), while non-canonical mutations outside of M41 (non-M41) result in reduced activity of both nuclear and cytoplasmic isoforms. Studies have reported clinical differences between canonical and non-canonical mutations, but these findings are constrained by small sample sizes and scarcity of genetic studies. In our study, we screened 29,000 individuals for UBA1 variants, referred for a broad range of hematologic diseases, and subjected to 62-gene panel sequencing, identifying 232 patients carrying likely disease-causing mutations. We identified decreased polyubiquitylation in all of the 18 UBA1 variants tested and found differences in H2A/B monoubiquitylation alteration between M41 and non-M41 mutations. Our findings confirm that patients harboring M41 mutations present at most with myelodysplastic neoplasms (MDS) and suggest that M41 mutations generally do not tolerate multiple co-mutations. In contrast, non-M41 mutations are more likely to appear with co-mutations and are detected in patients with hematologic neoplasms other than MDS. Our study establishes that M41 and non-M41 mutations exhibit distinct clinical and biological phenotypes, significantly enhancing UBA1 variant interpretation.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"33 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145254816","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}

引用次数: 0

Epigenetic dysregulation in Erdheim-Chester disease: perspectives from tissue and blood. 厄德海姆-切斯特病的表观遗传失调：来自组织和血液的观点。

IF 11.4 1区医学

Leukemia Pub Date : 2025-10-09 DOI: 10.1038/s41375-025-02785-2

Refael Meyuchas,Ofer Shpilberg,Oshrat Hershkovitz-Rokah

引用次数: 0

Divergent molecular pathways drive monomorphic epitheliotropic and enteropathy-associated intestinal T-cell lymphoma. 不同的分子通路驱动单纯性上皮性和肠病相关的肠t细胞淋巴瘤。

IF 11.4 1区医学

Leukemia Pub Date : 2025-10-07 DOI: 10.1038/s41375-025-02777-2

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

{"title":"Divergent molecular pathways drive monomorphic epitheliotropic and enteropathy-associated intestinal T-cell lymphoma.","authors":"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","doi":"10.1038/s41375-025-02777-2","DOIUrl":"https://doi.org/10.1038/s41375-025-02777-2","url":null,"abstract":"Enteropathy-associated intestinal T-cell lymphoma (EATL) and monomorphic epitheliotropic intestinal T-cell lymphoma (MEITL) have distinctive clinical context, morphology, and immunophenotype. To characterize their genetic and molecular specificities, we compared 30 EATLs and 52 MEITLs by whole-exome, RNA and miRNA sequencing and DNA methylation profiling. Highly recurrent SETD2 loss-of-function alterations and frequent mutations of H3-3A/B consistently altering H3R2, implying deregulation of histone marks, were selectively found in MEITL. EATL instead harbored frequent mutations in TET2, ARID1A, and KMT2D. Highly prevalent JAK-STAT pathway mutations preferentially affected JAK3 and STAT5B in MEITL, and JAK1 and STAT3 in EATL. Half of EATLs contained disruptive mutations in HLA class I genes, impacting class I molecule expression. EATL containing more abundant macrophages was enriched in inflammatory response signatures, with upregulation of CD274, CXCL13, and IDO1 transcripts, suggesting an immunosuppressive tumor microenvironment. CpGs hypomethylated in MEITL compared to EATL were enriched in promoter regions. Unsupervised analyses of mutations, transcription, and methylation profiles concordantly segregated EATLs from MEITLs. In summary, the distinctive genetic, epigenetic, and expression footprints of EATL and MEITL established by this study expand disease-defining features, have diagnostic implications, and provide a rationale for targeted therapies.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"21 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145240935","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}

引用次数: 0

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