Blood最新文献

{"title":"BLAST: A Globally Applicable and Molecularly Versatile Survival Model for Chronic Myelomonocytic Leukemia.","authors":"Ayalew Tefferi,Saubia Fathima,Maymona Abdelmagid,Ali Alsugair,Fnu Aperna,Mahsa Rezasoltani,Muhammad Yousuf,Anuya Natu,Clifford M Csizmar,Mark Gurney,Terra L Lasho,Christy M Finke,Rashmi Kanagal-Shamanna,Danielle Hammond,Kelly Sharon Chien,Alexandre Bazinet,Courtney D DiNardo,Tapan M Kadia,Abhishek A Mangaonkar,Naval G Daver,Animesh D Pardanani,Gautam Borthakur,Cinthya J Zepeda-Mendoza,Kaaren K Reichard,Rong He,Sanam Loghavi,Francesco Passamonti,Farhad Ravandi,Koji Sasaki,Dirk Larson,Guillermo Garcia-Manero,Francesco Onida,Naseema Gangat,Guillermo Montalban-Bravo,Mrinal M Patnaik","doi":"10.1182/blood.2024027170","DOIUrl":"https://doi.org/10.1182/blood.2024027170","url":null,"abstract":"We sought to develop a survival model in chronic myelomonocytic leukemia (CMML) that is primarily based on clinical variables and examine additional impact from mutations and karyotype. 457 molecularly-annotated patients were considered. Multivariable analysis identified circulating Blasts ≥2% (1 point), Leukocytes ≥13 x 109/L (1 point), and severe (2 points) or moderate (1 point) Anemia as preferred risk variables in developing a clinical risk Stratification Tool for overall survival (OS), acronymized to \"BLAST\": low-risk (0 points; median 63 months); intermediate-risk (1 point; median 28 months; HR 2.2, 95% CI 1.6-3.0), and high-risk (2-4 points; median 13 months; 5.4, 4.1-7.3); the corresponding 3/5 year OS rates were 68%/53%, 43%/18%, and 12%/1%. BLAST model performance (AUC 0.77/0.85 at 3/5-years) was shown to be comparable to that of the molecular CMML-specific prognostic scoring system (CMML-mol; AUC 0.73/0.75) and the international prognostic scoring system-molecular (IPSS-M; AUC 0.73/0.74). Multivariable analysis of mutations and karyotype identified PHF6MUT and TET2MUT as being \"favorable\" and DNMT3AMUT, U2AF1MUT, BCORMUT, SETBP1MUT, ASXL1MUT, NRASMUT, PTPN11MUT, RUNX1MUT, TP53MUT, and adverse karyotype, \"unfavorable\". Molecular information was subsequently encoded in a combined clinical-molecular risk model (BLAST-mol; AUC 0.80/0.86 at 3/5-years) that included the aforementioned BLAST clinical risk variables and a 3-tiered molecular risk score. BLAST and BLAST-mol were subsequently validated by two separate external cohorts. Independent risk factors for blast transformation included DNMT3AMUT, ASXL1MUT, PHF6WT, leukocytes ≥13 x 109/L, and ≥2% circulating or ≥10% bone marrow blasts. The current study proposes an easy to implement, globally applicable, and molecularly adaptive risk model for CMML.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"68 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143915084","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":"Phase 1/2 Study of High-Dose Palifermin for GVHD Prophylaxis in Patients Undergoing HLA-Matched Unrelated Donor HCT.","authors":"Eduard Schulz,Lauren M Curtis,Noa G Holtzman,Jennifer Sponaugle,Kaska Wloka,Alen Ostojic,Alain Mina,Najla El Jurdi,Filip Pirsl,Ashley Carpenter,Mahshid Golagha,Arlene Sirajuddin,Theo Heller,Brian C Shaffer,Frances T Hakim,Jeffrey Steven Rubin,Ronald E Gress,Steven Z Pavletic","doi":"10.1182/blood.2024028303","DOIUrl":"https://doi.org/10.1182/blood.2024028303","url":null,"abstract":"Graft-versus-host disease (GVHD) is a major complication of allogeneic hematopoietic cell transplantation (HCT). Palifermin, a recombinant N-truncated keratinocyte growth factor (KGF), protects epithelial tissues, including the thymus and gut. While high-dose KGF prevents GVHD in preclinical models, lower doses of palifermin were ineffective in humans. We conducted a phase 1/2 trial evaluating high-dose palifermin for preventing severe chronic GVHD (GVHD) in matched unrelated donor T-cell replete peripheral-blood HCT following reduced-intensity conditioning (RIC). Using a 3+3 design, we determined the recommended phase 2 dose (RP2D), followed by an expansion phase. Palifermin (180-720 μg/kg) was given on day -7 before HCT. All 31 patients received fludarabine/cyclophosphamide RIC with tacrolimus, methotrexate, and sirolimus for GVHD prophylaxis. Palifermin was well tolerated, with self-limiting rash and pancreatic enzyme elevations as notable grade 3/4 adverse events. The RP2D was 720 μg/kg. Remarkably, no patients at this dose developed grade II-IV acute GVHD (0/19), though severe chronic GVHD rates (primary endpoint) remained unchanged compared to historical controls. Post-transplant lymphocyte phenotyping suggests palifermin modulates Treg and naïve CD4+ T-cell numbers. These findings indicate high-dose palifermin with RIC is safe and may prevent acute GVHD, though it did not impact chronic GVHD rates in this study. NCT02356159.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"19 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143915088","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":"Delineating Mpl-dependent and -independent phenotypes of Jak2 V617F- positive MPNs in vivo.","authors":"Nicolas Papadopoulos,Audrey Nédélec,Yacine Rahmani,Hosuk Ryou,Jean-Philippe Defour,Jens Rittscher,Daniel Royston,Stefan N Constantinescu","doi":"10.1182/blood.2024026711","DOIUrl":"https://doi.org/10.1182/blood.2024026711","url":null,"abstract":"The Jak2 V617F mutation stands as the main driver of myeloproliferative neoplasms (MPNs) by constitutively activating signaling of several type I cytokine receptors, namely those for erythropoietin (EpoR), thrombopoietin (TpoR), and Granulocyte Colony Stimulating Factor (G-CSFR). Among these, TpoR assumes a pivotal role in hematopoietic stem cell renewal and differentiation, being positioned as a key driver of MPNs alongside mutated Jak2. However, the impact of TpoR/MPL absence in the context of Jak2 V617F in vivo has been explored only through a transgenic Jak2 V617F mouse model, where regulation of Jak2 expression does not depend on its natural promoter. In this study, we use a novel mouse model expressing Jak2 V617F under its endogenous promoter at the heterozygous state within a Mpl knock-out background. Our findings indicate that erythrocytosis, leukocytosis and moderate splenomegaly with mild spleen peri-vascular fibrosis persist even in the absence of Mpl expression. Notably, the inherent growth-stimulating effect induced by Jak2 V617F remains consistent across diverse early hematopoietic progenitor populations in the absence of Mpl but is reduced at the stem cell level and does not allow clonal expansion in competitive transplantation. Our results delineate Mpl-dependent and -independent phenotypes induced by Jak2 V617F and confirm that inhibiting Mpl expression at the stem cell level negates the long-term advantage of the mutant clone. Consequently, while MPL emerges as a major player in Jak2 V617F positive MPNs, our study underscores that it is not the exclusive contributor, broadening the spectrum for therapeutic intervention.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"65 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143915087","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":"Menin inhibition with revumenib for NPM1-mutated relapsed or refractory acute myeloid leukemia: the AUGMENT-101 study.","authors":"Martha L Arellano,Michael J Thirman,John F DiPersio,Mael Heiblig,Eytan M Stein,Andre C Schuh,Andrius Zucenka,Stéphane De Botton,Carolyn S Grove,Gabriel N Mannis,Cristina Papayannidis,Alexander E Perl,Ghayas C Issa,Ibrahim Aldoss,Ashish Bajel,David S Dickens,Michael W M Kühn,Ioannis Mantzaris,Emmanuel Raffoux,Elie Traer,Irina Amitai,Hartmut Döhner,Corinna Greco,Tibor J Kovacsovics,Christine M McMahon,Pau Montesinos,Arnaud Pigneux,Paul J Shami,Richard M Stone,Ofir Wolach,John G Harpel,Yakov Chudnovsky,Li Yu,Rebecca G Bagley,Angela R Smith,James S Blachly","doi":"10.1182/blood.2025028357","DOIUrl":"https://doi.org/10.1182/blood.2025028357","url":null,"abstract":"The prognosis for relapsed or refractory (R/R) nucleophosmin 1-mutated (NPM1m) acute myeloid leukemia (AML) is poor and represents an urgent unmet medical need. Revumenib, a potent, selective menin inhibitor, was recently approved for the treatment of R/R acute leukemia with a KMT2A translocation in patients aged ≥1 year based on results from the phase 1/2 AUGMENT-101 study. Here we present results from patients with R/R NPM1m AML enrolled in the phase 2 portion of AUGMENT-101. Enrolled patients received revumenib with or without a strong CYP3A4 inhibitor every 12 hours in 28-day cycles. Primary endpoints were rate of complete remission (CR) or CR with partial hematologic recovery (CRh; CR+CRh), and safety and tolerability. Secondary endpoints included overall response rate (ORR) and duration of response. As of September 18, 2024, 84 patients received ≥1 dose of revumenib. Median age was 63 years; 1 patient was aged <18 years. The protocol-defined efficacy-evaluable population for the primary analysis included 64 adult patients (≥3 prior lines of therapy, 35.9%; prior venetoclax, 75.0%). The CR+CRh rate was 23.4% (1-sided P=.0014); the ORR was 46.9%. Median duration of CR+CRh was 4.7 months. Five of 30 responders (16.7%) proceeded to hematopoietic stem cell transplant (HSCT); 3 resumed revumenib after HSCT. Treatment-related adverse events led to treatment discontinuation in 4 patients (4.8%). Revumenib demonstrated clinically meaningful responses in this heavily pretreated, older population with NPM1m AML, including remissions that enabled HSCT. The safety profile of revumenib was consistent with previously reported results. This trial was registered at www.clinicaltrials.gov as NCT04065399.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"2 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143915085","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 CD38 with Daratumumab for Platelet Transfusion Refractoriness in Aplastic Anemia.","authors":"Zhen Gao,Hong Pan,Lele Zhang,Weiwang Li,Ruonan Li,Jingyu Zhao,Yuechen Luo,Yu Lian,Xiao Yu,Zhexiang Kuang,Neng Nie,Jianping Li,Jinbo Huang,Xin Zhao,Yuan Li,Liwei Fang,Meili Ge,Yizhou Zheng,Jun Shi","doi":"10.1182/blood.2025029006","DOIUrl":"https://doi.org/10.1182/blood.2025029006","url":null,"abstract":"We found that 8 out of 10 aplastic anemia patients experienced resolution of platelet transfusion refractoriness following daratumumab administration. Notably, 4 responders achieved hematopoietic recovery, including 3 participants showed improvements in multi-lineage blood cell counts, even with daratumumab monotherapy (NCT05832216).","PeriodicalId":9102,"journal":{"name":"Blood","volume":"11 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143915044","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":"A multiomic analysis of Waldenström macroglobulinemia defines distinct disease subtypes.","authors":"Dylan C Gagler,Hussein Ghamlouch,Di Zhang,Patrick Blaney,Avital Tenenbaum,James Blake Langton,Marine Armand,Alexandre Eeckhoutte,Amina Joudat,Michaël Degaud,Michela Esposito,Gaurav Varma,Yubao Wang,Sanghoon Lee,Sanxiong Liu,Oscar B Lahoud,David Kaminetzky,Marc J Braunstein,Louis Williams,Florence Nguyen-Khac,Brian A Walker,Damien Roos-Weil,Faith E Davies,Olivier A Bernard,Gareth J Morgan","doi":"10.1182/blood.2024028164","DOIUrl":"https://doi.org/10.1182/blood.2024028164","url":null,"abstract":"We carried out a single-cell (sc) multiomic analysis on a series of MYD88 mutated Waldenström macroglobulinemia (WM) cases and identified two distinct subtypes of disease, memory B-cell-like (MBC-like) and plasma cell-like (PC-like), based on their expression of key lineage defining genes. Biologically, the subtypes are characterized by their variable capacity to differentiate fully towards a plasma cell (PC) and exhibit unique transcriptomic, chromatin accessibility, and genomic profiles. The MBC-like subtype is unable to differentiate beyond the memory B-cell (MBC) stage, upregulates key MBC genes, and is characterized by upregulated BCR and AKT/mTOR signaling. In contrast, the PC-like subtype can partially differentiate towards a PC, upregulates key PC genes, has enhanced NF-kB signaling, and has an upregulated unfolded protein response. Pseudotime trajectory analysis of combined scRNA-sequencing and scATAC-sequencing supports the variable differentiation capacity of each subtype and implicate key transcription factors SPI1, SPIB, BCL11A, and XBP1 in these features. The existence and generalizability of the two disease subtypes were validated further using hierarchical clustering of bulk RNA-seq data from a secondary set of cases. The biological significance of the subtypes was further established using whole genome sequencing, where it was shown that CXCR4, NIK, and ARID1A mutations occur predominantly in the MBC-like subtype and 6q deletions in the PC-like subtype. We conclude that the variable differentiation blockade seen in WM manifests itself clinically as two disease subtypes with distinct epigenetic, mutational, transcriptional, and clinical features with potential implications for WM treatment strategies.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"115 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143915082","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":"How I treat higher-risk MDS.","authors":"Alain Mina, Rami Komrokji","doi":"10.1182/blood.2024025271","DOIUrl":"10.1182/blood.2024025271","url":null,"abstract":"<p><strong>Abstract: </strong>Myelodysplastic syndromes/neoplasms (MDS) are a widely heterogenous group of myeloid malignancies characterized by morphological dysplasia, a defective hematopoiesis, and recurrent genetic abnormalities. The original International Prognostic Scoring System (IPSS) and revised IPSS have been used to risk-stratify patients with MDS to guide treatment strategies. In higher-risk MDS, the therapeutic approach is geared toward delaying leukemic transformation and prolonging survival. For more than a decade, the hypomethylating agents azacitidine and decitabine have been the standard of care and, when feasible, an allogeneic hematopoietic stem cell transplantation should be considered. However, the IPSS scoring systems solely rely on clinical, morphological, and cytogenetic features and do not account for somatic mutations present in >80% of cases. These genetic abnormalities have been shown to play a crucial role in prognostication, prompting the development of molecular IPSS, and the integration of genomic features into MDS classification systems in recent years. In this review, we delineate our approach to higher-risk MDS in the context of updated classifications and the latest prognostication tools. We use illustrative clinical cases to support our discussion and share insights from recent clinical trials, highlighting lessons learned.</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"2002-2011"},"PeriodicalIF":21.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982874","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":"Reactive oxygen species regulate early development of the intestinal macrophage-microbiome interface.","authors":"Zohreh Mansoori Moghadam, Bei Zhao, Candice Raynaud, Valentina Strohmeier, Jana Neuber, Anne Kathrin Lösslein, Sabrina Qureshi, Vitka Gres, Tara Ziegelbauer, Sebastian Baasch, Christoph Schell, Klaus Warnatz, Naohiro Inohara, Gabriel Nuñez, Thomas Clavel, Stephan P Rosshart, Julia Kolter, Philipp Henneke","doi":"10.1182/blood.2024025240","DOIUrl":"10.1182/blood.2024025240","url":null,"abstract":"<p><strong>Abstract: </strong>The controlled development of cellular intestinal immunity in the face of dynamic microbiota emergence constitutes a major challenge in very early life and is a bottleneck for sustained growth and well-being. Early-onset inflammatory bowel disease (IBD) represents an extreme disturbance of intestinal immunity. It is a hallmark and often the first manifestation of chronic granulomatous disease (CGD), caused by inborn defects in the nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) in phagocytes and thus the failure to produce reactive oxygen species (ROS). However, in contrast to the known role of ROS in antimicrobial defense, the mechanisms underlying intestinal immunopathology in CGD remain enigmatic. This is partly due to the incomplete recapitulation of the CGD-IBD phenotype in established mouse models. We found that mice deficient in the NOX2 subunits p47phox or gp91phox showed similar baseline disturbances in lamina propria macrophage differentiation but responded differently to chemically induced colitis. Although p47phox- and gp91phox-deficient mice differed markedly in microbiota composition, crossfostering failed to equalize discrepant IBD phenotypes and microbiota, pointing at extremely early and functionally important microbiota fixation under specific pathogen-free housing conditions. In contrast, neonatal acquisition of a complex wild-mouse microbiota triggered spontaneous IBD, granuloma formation, and secondary sepsis with intestinal pathogens in both NOX2-deficient mouse lines, which was in part dependent on NOX2 in intestinal macrophages. Thus, in experimental CGD, the aberrant development of tissue immunity and microbiota are closely intertwined immediately after birth.</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"2025-2040"},"PeriodicalIF":21.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122308","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":"Decoding functional hematopoietic progenitor cells in the adult human lung.","authors":"Catharina Conrad, Mélia Magnen, Jessica Tsui, Harrison Wismer, Mohammad Naser, Urmila Venkataramani, Bushra Samad, Simon J Cleary, Longhui Qiu, Jennifer J Tian, Marco De Giovanni, Nicole Mende, Andrew D Leavitt, Emmanuelle Passegué, Elisa Laurenti, Alexis J Combes, Mark R Looney","doi":"10.1182/blood.2024027884","DOIUrl":"10.1182/blood.2024027884","url":null,"abstract":"<p><strong>Abstract: </strong>Although the bone marrow is the main site of blood cell production in adults, rare pools of hematopoietic stem and progenitor cells have been found in extramedullary organs. In mice, we have previously shown that the lung contains hematopoietic progenitor cells and is a site of platelet production. Here, in the adult human lung, we show that functional hematopoietic precursors reside in the extravascular spaces with a frequency similar to the bone marrow and are capable of proliferation and engraftment in mice. The gene signature of pulmonary and medullary CD34+ hematopoietic progenitors indicates greater baseline activation of immune-, megakaryocyte/platelet-, and erythroid-related pathways in lung progenitors. Spatial transcriptomics mapped blood progenitors in the lung to an alveolar interstitium niche with only a few cells identified in an intravascular location. In human blood samples collected for stem cell transplantation, CD34+ cells with a lung signature enriched the mobilized pool of hematopoietic stem cells. These results identify the lung as a pool for uniquely programmed blood stem and progenitor cells with the potential to support hematopoiesis in humans.</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"1975-1986"},"PeriodicalIF":21.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7617544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522538","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}

{"title":"Donor regulatory/conventional T-cell grafts for the GVHD win?","authors":"Antonio Pierini,John Koreth","doi":"10.1182/blood.2024028047","DOIUrl":"https://doi.org/10.1182/blood.2024028047","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"36 1","pages":"1964-1965"},"PeriodicalIF":20.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143897459","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}