Blood最新文献

{"title":"Project EVOLVE: An international analysis of postimmunotherapy lineage switch, an emergent form of relapse in leukemia.","authors":"Sara K Silbert, Alexander W Rankin, Chloe N Hoang, Alexandra Semchenkova, Regina M Myers, Elena Zerkalenkova, Hao-Wei Wang, Alexandra E Kovach, Constance M Yuan, Dana Delgado Colon, Loic Vasseur, Alex Bataller, Samuel John, Kaylyn Utley Lyons, Barbara D Friedes, Anna Alonso-Saladrigues, Hisham Abdel-Azim, Estelle Balducci, Ahmed Aljudi, Marie Balsat, D Nathan Biery, Aghiad Chamdin, Bill H Chang, Raymund S Cuevo, Barbara De Moerloose, David S Dickens, Ulrich A Duffner, Nicolas Duployez, Firas El Chaer, Michelle Ann Elliott, Gabriele Escherich, Sneha Fernandes, Mandi R Fitzjohn, Zhubin J Gahvari, Stephan A Grupp, Rui Rochelle He, Cynthia Harrison, Christopher Bruce Hergott, Emily M Hsieh, Annette S Kim, Dennis John Kuo, Daniel P Larson, Benjamin J Lee, Thibaut Tl Leguay, R Coleman Lindsley, Abhishek A Mangaonkar, Kerstin Mezger, Holly L Pacenta, Jing Pan, Marlie R M Provost, Latika Puri, Sunil Sudhir Raikar, Armando Jose Martinez, Isabella Quijada Bristol, Kyle Daniel Murphy, Lauren Reiman, Michele S Redell, Kelly Reed, Gabrielle Roth Guepin, Jeremy D Rubinstein, Süreyya Savaşan, Kristian T Schafernak, Alexandra McLean Stevens, Aimee C Talleur, Naomi Torres Carapia, Jacques Vargaftig, Anant Vatsayan, Matthias Wölfl, Lipng Zhao, Susana Rives, Vanessa A Fabrizio, Koji Sasaki, Ibrahim Aldoss, Nicolas Boissel, Susan R Rheingold, Kara L Davis, Sara Ghorashian, Elad Jacoby, Alexander Popov, Adam Joseph Lamble, Nirali N Shah","doi":"10.1182/blood.2024026655","DOIUrl":"https://doi.org/10.1182/blood.2024026655","url":null,"abstract":"<p><p>Lineage switch (LS), defined as the immunophenotypic transformation of acute leukemia, has emerged as a mechanism of relapse following antigen-targeted immunotherapy which is associated with dismal outcomes. Through an international collaborative effort, we identified cases of LS following a host of antigen-targeted therapies (e.g., CD19, CD22, CD38 and CD7), described how LS was diagnosed, reviewed treatment approaches, and analyzed overall outcomes for this form of post-immunotherapy relapse. Collectively, 75 cases of LS were evaluated, including 53 (70.7%) cases of B-ALL to AML, 17 (22.7%) cases of B-ALL to mixed phenotypic acute leukemia (MPAL)/acute leukemias of ambiguous lineage (ALAL), and 5 (6.7%) cases of rare LS presentation (i.e., T-cell ALL to AML). An additional 10 cases with incomplete changes in immunophenotype, referred to as \"lineage drift\" were also described. With a primary focus on the 70 cases of LS from B-ALL to AML or MPAL/ALAL, LS emerged at a median of 1.5 months (range, 0-36.5 months) post-immunotherapy, with 81.4% presenting with LS within the first 6 months from the most proximal immunotherapy. While the majority involved KMT2A rearrangements (n=45, 64.3%), other rare cytogenetic and/or molecular alterations were uniquely observed. Treatment outcomes were generally poor with < 40% remission rates. The median overall survival following LS diagnosis was 4.8 months. Outcomes were similarly poor for those with rare immunophenotypes of LS or \"lineage drift.\" This global initiative robustly categorizes lineage changes post-immunotherapy and, through enhanced understanding, establishes a foundation for improving outcomes of LS.</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802462","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":"Two strikes, base hit: odronextamab after CAR T cells in LBCL.","authors":"Jason Westin","doi":"10.1182/blood.2024027961","DOIUrl":"https://doi.org/10.1182/blood.2024027961","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"145 14","pages":"1441-1442"},"PeriodicalIF":21.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771234","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":"CD44-mediated metabolic rewiring is a targetable dependency of IDH-mutant leukemia.","authors":"Junhua Lyu, Yuxuan Liu, Ningning Liu, Hieu S Vu, Feng Cai, Hui Cao, Pranita Kaphle, Zheng Wu, Giovanni A Botten, Yuannyu Zhang, Jin Wang, Sarada Achyutuni, Xiaofei Gao, Ilaria Iacobucci, Charles G Mullighan, Stephen S Chung, Min Ni, Ralph J DeBerardinis, Jian Xu","doi":"10.1182/blood.2024027207","DOIUrl":"10.1182/blood.2024027207","url":null,"abstract":"<p><strong>Abstract: </strong>Recurrent isocitrate dehydrogenase (IDH) mutations catalyze nicotinamide adenine dinucleotide phosphate (NADPH)-dependent production of oncometabolite (R)-2-hydroxyglutarate (R-2HG) for tumorigenesis. IDH inhibition provides clinical response in a subset of acute myeloid leukemia (AML) cases; however, most patients develop resistance, highlighting the need for more effective IDH-targeting therapies. By comparing transcriptomic alterations in isogenic leukemia cells harboring CRISPR base-edited IDH mutations, we identify the activation of adhesion molecules including CD44, a transmembrane glycoprotein, as a shared feature of IDH-mutant leukemia, consistent with elevated CD44 expression in IDH-mutant AML patients. CD44 is indispensable for IDH-mutant leukemia cells through activating pentose phosphate pathway and inhibiting glycolysis by phosphorylating glucose-6-phosphate dehydrogenase and pyruvate kinase muscle isozyme M2, respectively. This metabolic rewiring ensures efficient NADPH generation for mutant IDH-catalyzed R-2HG production. Combining IDH inhibition with CD44 blockade enhances the elimination of IDH-mutant leukemia cells. Hence, we describe an oncogenic feedforward pathway involving CD44-mediated metabolic rewiring for oncometabolite production, representing a potentially targetable dependency of IDH-mutant malignancies.</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"1553-1567"},"PeriodicalIF":21.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000142","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":"Prizloncabtagene autoleucel: a new CAR T cell for B-NHL.","authors":"Alberto Mussetti, Anna Sureda","doi":"10.1182/blood.2024028030","DOIUrl":"https://doi.org/10.1182/blood.2024028030","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"145 14","pages":"1444-1445"},"PeriodicalIF":21.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771271","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":"Chromoplexy and FNDC3B::RARB fusion: deciphering a rare case of PML::RARA-negative APL.","authors":"Audrey Bidet, Emilie Klein","doi":"10.1182/blood.2024027991","DOIUrl":"https://doi.org/10.1182/blood.2024027991","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"145 14","pages":"1588"},"PeriodicalIF":21.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771088","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":"iPSCs unlock clues to pediatric AML onset.","authors":"Cornelis Jan Pronk, Charlotta Böiers","doi":"10.1182/blood.2024027101","DOIUrl":"https://doi.org/10.1182/blood.2024027101","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"145 14","pages":"1442-1444"},"PeriodicalIF":21.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771270","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":"The immunotherapy real estate of Hodgkin lymphoma.","authors":"Christian Steidl","doi":"10.1182/blood.2024027782","DOIUrl":"https://doi.org/10.1182/blood.2024027782","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"145 14","pages":"1445-1447"},"PeriodicalIF":21.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771273","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":"Giant cytoplasmic inclusions (Alder-Reilly bodies) in Hurler syndrome (mucopolysaccharidosis type 1H).","authors":"Bhaumik Shah, Gerald B Wertheim","doi":"10.1182/blood.2024025158","DOIUrl":"https://doi.org/10.1182/blood.2024025158","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"145 14","pages":"1589"},"PeriodicalIF":21.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771090","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":"\"When I'm 64\": functional shift of aging platelets.","authors":"Laura Gutiérrez","doi":"10.1182/blood.2024027996","DOIUrl":"https://doi.org/10.1182/blood.2024027996","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"145 14","pages":"1447-1449"},"PeriodicalIF":21.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771086","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":"Classification and risk stratification in T-lineage acute lymphoblastic leukemia.","authors":"Petri Pölönen, Charles G Mullighan, David T Teachey","doi":"10.1182/blood.2023022920","DOIUrl":"10.1182/blood.2023022920","url":null,"abstract":"<p><strong>Abstract: </strong>Cure rates for patients with acute lymphoblastic leukemia (ALL) have improved markedly in recent decades, in part because of risk stratification incorporating leukemia genomics, response to treatment, and clinical features to be able to determine at diagnosis which patients are more likely to relapse or have refractory disease. Although risk stratification is well developed for patients with B-lineage ALL, it remains challenging for those with T-lineage ALL (T-ALL). Prognostic factors validated across clinical trials and real-world data in T-ALL include age, central nervous system involvement, and measurable residual disease (MRD) response. Immunophenotype, including early T-cell precursor ALL, is widely used to classify T-ALL but is not consistently associated with outcome in multivariable risk models. Historically, few genetic alterations have been consistently associated with outcome, but recent comprehensive, large-scale genomic profiling has identified multiple genetic subtypes and alterations associated with outcome independent of MRD. This review highlights ongoing efforts to identify reliable prognostic biomarkers and underscores the potential of genomics-based classification to guide future T-ALL treatment strategies.</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"1464-1474"},"PeriodicalIF":21.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364342","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}