Blood最新文献

{"title":"Final analysis of the RESONATE-2 study: up to 10 years of follow-up of first-line ibrutinib treatment for CLL/SLL.","authors":"Jan A Burger,Paul M Barr,Tadeusz Robak,Carolyn Owen,Alessandra Tedeschi,Anita Sarma,Piers Em Patten,Sebastian Grosicki,Helen McCarthy,Fritz Offner,Edith Szafer Glusman,Cathy Zhou,Anita Szoke,Lynne Neumayr,James P Dean,Paolo Ghia,Thomas Kipps","doi":"10.1182/blood.2024028205","DOIUrl":"https://doi.org/10.1182/blood.2024028205","url":null,"abstract":"With up to 10 years of follow-up, we report results from the final analysis of RESONATE-2 (NCT01722487/NCT01724346), a phase 3 study of first-line ibrutinib versus chlorambucil for the treatment of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL). Patients aged ≥65 years with previously untreated CLL/SLL without del(17p) were randomly assigned to receive either single-agent ibrutinib (420 mg/day; n = 136) or chlorambucil (0.5-0.8 mg/kg ≤12 cycles; n = 133) until disease progression/unacceptable toxicity. With a median follow-up of 9.6 in the ibrutinib arm, median PFS was 8.9 years (95% CI, 7.0-NE) versus 1.3 years (95% CI, 0.9-1.6) for the chlorambucil arm. Among patients with unmutated IGHV, del(11q), mutated TP53, or complex karyotype median PFS was 8.4 years (95% CI, 6.8-NE) with ibrutinib and 0.7 years (95% CI, 0.4-1.2) with chlorambucil. Median overall survival (OS) with ibrutinib was not reached. Most common adverse events (AEs) of any grade included diarrhea (52%), fatigue (41%), cough (39%), nausea (32%), arthralgia (31%), peripheral edema (31%), and hypertension (30%). During the entire study period, 34/136 patients (25%) had an ibrutinib dose reduction due to AEs; these AEs improved in 30/34 patients (88%). At study completion, 27% of patients remained on first-line ibrutinib treatment. With the longest follow-up to date from a phase 3 study of any targeted CLL/SLL therapy, this landmark RESONATE-2 study defines median PFS and demonstrates continued OS benefit of first-line ibrutinib treatment for patients with CLL/SLL, including those with high-risk genomic features. Sustained efficacy and tolerability of ibrutinib reemphasize the favorable benefit-risk profile.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"143 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747880","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":"Disease risk but not remission status determines transplant outcomes in AML: long-term outcomes of the ASAP trial.","authors":"Matthias Stelljes,Jan Moritz Middeke,Gesine Bug,Eva Maria Wagner-Drouet,Lutz P Mueller,Christoph Schmid,Stefan W Krause,Wolfgang Andreas Bethge,Edgar Jost,Uwe Platzbecker,Stefan Klein,Judith Niederland,Martin Kaufmann,Kerstin Schäfer-Eckart,Henning Baldauf,Friedrich Stölzel,Sarah Trost,Christoph Röllig,Malte von Bonin,Katharina Egger-Heidrich,Desiree Kunadt,Björn Steffen,Beate Hauptrock,Christoph Schliemann,Katja Sockel,Fabian Lang,Oliver Kriege,Judith Schaffrath,Christian Reicherts,Wolfgang E Berdel,Hubert Serve,Gerhard Ehninger,Alexander H Schmidt,Jan-Henrik Mikesch,Martin Bornhäuser,Johannes Schetelig","doi":"10.1182/blood.2025028730","DOIUrl":"https://doi.org/10.1182/blood.2025028730","url":null,"abstract":"Attempting to induce a complete remission (CR) prior to allogeneic hematopoietic cell transplantation (alloHCT) is current practice in patients with AML. A benefit of remission induction prior to alloHCT, however, has never been proven in a prospective trial. Potent conditioning regimens exist which allow for successful alloHCT in patients with active AML. Therefore, the ASAP trial was conducted to test remission induction by salvage chemotherapy prior to alloHCT against immediate transplantation after intensified conditioning. In total 281 patients with AML with poor response after first induction or untreated first relapse were randomized 1:1 to remission induction (RIST) with high-dose cytarabine plus mitoxantrone versus immediate alloHCT with sequential conditioning after non-intensive disease control measures (DisC) preferentially watchful waiting only. Overall survival (OS) at 5 years from randomization analyzed according to ITT was 46.1% for DisC versus 47.5% for RIST (p=0.82). In multivariable Cox regression analysis, genetic AML risk according to ELN (p<0.0001), age (p=0.001) and comorbidities (p=0.046) predicted survival, but not treatment arm (HR 1.08 for DisC versus RIST, p=0.67). In conclusion, long-term follow-up of the ASAP trial showed no survival advantage for standard salvage chemotherapy prior to alloHCT as opposed to immediate alloHCT. The trial results question the general concept of remission induction with intensive standard salvage therapy prior to alloHCT for all patients, since immediate alloHCT may reduce time in hospital and health care expenses. Well tolerable novel bridging therapies and post-transplant maintenance with targeted drugs are urgently warranted, especially for adverse-risk AML, to improve outcome after alloHCT. NCT02461537.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"25 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747885","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":"New prognostic systems for multiple myeloma in the context of contemporary therapies.","authors":"Andrew Spencer","doi":"10.1182/blood.2024023841","DOIUrl":"https://doi.org/10.1182/blood.2024023841","url":null,"abstract":"Recent clinical trials in both transplant eligible and ineligible newly diagnosed multiple myeloma utilising three and four drug combinations have demonstrated unprecedented levels of response. However, two recently published studies redefining high-risk in newly diagnosed multiple myeloma in the context of these newer and more effective treatments demonstrate that a significant minority of patients likely derive little benefit from these newer approaches. These new prognostic systems thus provide an evidence-based framework for the development of much needed risk-stratified clinical trials.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"8 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747821","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":"XPO1 Drives Resistance to Eprenetapopt and Azacitidine and Can Be Targeted in TP53-Mutated Myeloid Malignancies.","authors":"Traci L Kruer,Ariel Quintana-Gonzalez,Hannah L Newman,Meghan C Ferrall-Fairbanks,Ling Zhang,Amy F McLemore,Surendra Neupane,Qin Yang,Nana Adjoa Ben-Crentsil,Maria E Balasis,Christopher T Letson,Rami S Komrokji,Sana Chaudhry,Tulasigeri M Totiger,Joshua A Traina,Maria E Figueroa,Christopher B Ryder,Thomas Cluzeau,Justin Taylor,David A Sallman,Eric Padron","doi":"10.1182/blood.2025028803","DOIUrl":"https://doi.org/10.1182/blood.2025028803","url":null,"abstract":"TP53 mutated myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) are among the most aggressive and chemotherapy refractory myeloid neoplasms with a median overall survival of less than 6 months. An enormous unmet need exists to develop novel therapeutic strategies and understand resistance mechanisms to suboptimal existing therapies for this disease. In two parallel phase 2 clinical trials that combined eprenetapopt with azacitidine in TP53 mutated MDS/AML, we observed complete remission rates of 40-50% and molecular remission rates of 38%. However, unless allogeneic stem cell transplantation was performed, relapse inevitably occurred. To understand the mechanisms of secondary resistance responsible for this, we genotyped sequential clinical trial samples, conducted a genome-wide CRISPR screen in TP53 mutated leukemia cells, and identified XPO1 as a therapeutically tractable mediator of resistance. We demonstrate that XPO1 is overexpressed in patient samples after eprenetapopt and azacitidine treatment, elucidate the mechanism by which this occurs, and determine that it is necessary and sufficient for resistance to combination therapy. Finally, we validate in a variety of model systems including a novel patient derived xenograft model of TP53 mutant MDS, that eprenetapopt in combination with XPO1 inhibitors can overcome this resistance, providing preclinical rationale that this novel combination strategy is a viable therapeutic approach in TP53 mutant MDS/AML patients.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"718 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747889","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":"Time to complete remission is an independent determinant of survival after intensive chemotherapy in AML.","authors":"Rithin Nedumannil,Michael Ashby,James P Rowland,Jacques A J Malherbe,Jared Fairbank,Kelli Gray,Sun Loo,Matthew Wright,John Reynolds,Devendra K Hiwase,Paula Marlton,Shaun A Fleming,Ashish Bajel,Andrew H Wei","doi":"10.1182/blood.2025028594","DOIUrl":"https://doi.org/10.1182/blood.2025028594","url":null,"abstract":"The purpose of this study was to explore and determine the optimal landmark for defining complete remission after intensive induction therapy that best correlates with long-term survival outcome among patients with newly diagnosed acute myeloid leukemia (AML).","PeriodicalId":9102,"journal":{"name":"Blood","volume":"1 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144737223","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 clinical guide to TP53 mutations in myeloid neoplasms.","authors":"Samuel Urrutia,Terrence N Wong,Daniel C Link","doi":"10.1182/blood.2025029691","DOIUrl":"https://doi.org/10.1182/blood.2025029691","url":null,"abstract":"TP53 mutations are found in 10-15% of myeloid neoplasms and are one of its most important prognostic factors. Emerging data show that TP53 mutational allele status is a key determinant of clinical outcomes, with multi-hit TP53 mutant myeloid neoplasms having a very poor prognosis. Significant differences exist among the methods used in clinical and research settings to assess TP53 mutational status, leading to variability in reported patient characteristics, response to therapy, and survival. Indeed, differences in the criteria used to define TP53 mutational states among professional societies and in landmark research studies have led to confusion, suboptimal clinical testing, and variability in therapy recommendations. We review the methods used to assess for TP53 mutational allele status and provide recommendations, based on clinically available testing, for the accurate evaluation of TP53 gene mutations in myeloid neoplasms. Hotspot mutations represent ~35% of all TP53 missense mutations in myeloid neoplasms. There is evidence that these hotspot mutations may have dominant-negative or gain-of function properties. Here, we review this evidence and discuss the potential impact of TP53 mutation identity on patient outcomes and clinical management.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"9 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144737258","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":"Casein kinase 1α essentially regulates thrombopoiesis by driving megakaryocyte maturation and cytoskeleton organization.","authors":"Ferdinand Kollotzek,Kristina Mott,Melina Fischer,Betül Findik,Vanessa Göb,Mailin-Christin Manke,Carla Emilia Borst,Amin Polzin,Martin D Burkhalter,Anita E Eckly,Tamam Bakchoul,Melanie Philipp,Samuel Josua Holzmayer,Leticia Quintanilla-Fend,Claudia Lengerke,Meinrad Gawaz,Catherine Leon,David Stegner,Bernhard Nieswandt,William Vainchenker,Markus Bender,Julia Skokowa,Harald Schulze,Patrick Münzer,Oliver Borst","doi":"10.1182/blood.2025028460","DOIUrl":"https://doi.org/10.1182/blood.2025028460","url":null,"abstract":"Throughout thrombopoiesis megakaryocytes (MKs) form proplatelets within the bone marrow (BM) and release platelets into BM sinusoids. Casein Kinase 1α (CK1α) is a major player and, thus an important therapeutic target in several hematological malignancies. This study aims to define the role of CK1α for the essential steps of thrombopoiesis and to dissect potential mechanisms of thrombocytopenia. MK-specific CK1α-deficiency resulted in a macrothrombocytopenia. Ck1αPf4Δ/Pf4Δ mice displayed a substantial BM hyperplasia with pivotal changes in MK nuclear lobulation and reduced contact to BM sinusoids. Ck1αPf4Δ/Pf4Δ MKs displayed a defective cytoskeleton organization reflected by a decreased amount of polymerized F-actin and disturbed microtubule dynamics due to p21/p53 accumulation and impaired ROCK/LIMK/cofilin signaling. Further, pronounced defects in DMS polarization and proplatelet formation of Ck1αPf4Δ/Pf4Δ MKs unraveled CK1α as a prerequisite for thrombopoiesis. Our findings could be translated into a human approach, since a CRISPR/Cas9-mediated genetic deletion of CSNK1A1 in MKs derived from human CD34+ progenitor cells resulted in a substantial defect in human MK maturation and platelet production. The present observations elucidated CK1α as an important signaling molecule in MK cytoskeletal dynamics and polarization, proplatelet formation and polyploidization, thus highlighting the crucial role of CK1α in platelet biogenesis.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"7 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144737260","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":"Enhancer heterogeneity in acute lymphoblastic leukemia drives differential gene expression in patients.","authors":"Alastair Smith, Nicholas David Robert Denny, Catherine Chahrour, Kim Sharp, Marta Arachi, Ana Maria Dopico-Fernandez, Natalina Elliott, Joe Harman, Thomas Jackson, Huimin Geng, Owen Smith, Jonathan Bond, Irene Roberts, Ronald W W Stam, Nicholas Crump, James Davies, Anindita Roy, Thomas A Milne","doi":"10.1182/blood.2024028019","DOIUrl":"https://doi.org/10.1182/blood.2024028019","url":null,"abstract":"<p><p>Genetic alterations alone cannot account for the diverse phenotypes of cancer cells. Even cancers with the same driver mutation show significant transcriptional heterogeneity and varied responses to therapy. However, the mechanisms underpinning this heterogeneity remain under-explored. Here, we find that novel enhancer usage is a common feature in acute lymphoblastic leukemia (ALL). In particular, KMT2A::AFF1 ALL, an aggressive leukemia with a poor prognosis and a low mutational burden, exhibits substantial transcriptional heterogeneity between individuals. Using single cell multiome analysis and extensive chromatin profiling, we reveal that much transcriptional heterogeneity in KMT2A::AFF1 ALL is driven by novel enhancer usage. By generating high resolution Micro Capture-C data in primary patient samples, we identify patient-specific enhancer activity at key oncogenes such as MEIS1 and RUNX2, driving high levels of expression of both oncogenes in a patient-specific manner. Overall, our data show that enhancer heterogeneity is highly prevalent in KMT2A::AFF1 ALL and may be a mechanism that drives transcriptional heterogeneity in cancer more generally.</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":""},"PeriodicalIF":23.1,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144741173","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 patients with CLL after prior treatment with a covalent BTK inhibitor and a BCL-2 inhibitor.","authors":"Mazyar Shadman,Matthew S Davids","doi":"10.1182/blood.2024025482","DOIUrl":"https://doi.org/10.1182/blood.2024025482","url":null,"abstract":"The treatment landscape for chronic lymphocytic leukemia (CLL) has been revolutionized by the advent of novel agents, particularly covalent BTK inhibitors (cBTKis) and BCL-2 inhibitors (BCL-2is). This has resulted in significant improvement in outcome of patients with CLL many of whom experience a life expectancy comparable to general population. However, patients who are double-refractory, having progressed following exposure to both classes face limited options and poor outcomes. This manuscript presents a practical approach to managing double-exposed or double-refractory CLL, integrating clinical case discussions, trial data, and expert insights. For patients with intolerance to cBTKis, second-generation agents may remain effective. Similarly, re-treatment with venetoclax can be considered after prior fixed-duration use. In double-refractory disease, the non-covalent BTK inhibitor (e.g., pirtobrutinib) and CD19-directed CAR-T therapy (lisocabtagene maraleucel) are available standard-of-care options. Pirtobrutinib provides rapid disease control but often with limited durability, emphasizing the importance of early planning for consolidation with CAR-T or allogeneic stem cell transplant. Persistent disease after CAR-T warrants close follow-up and timely referral for transplant evaluation in eligible patients. While PI3K inhibitors are also available, their role is limited due to toxicity and modest efficacy. Investigational agents-including BTK degraders, bispecific antibodies, and novel cellular therapies-offer promise for the future. A nuanced, individualized treatment strategy that incorporates current therapies and emerging options is essential to optimize outcomes in double-refractory CLL.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"15 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144737259","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":"Impaired cytotoxic function and exhausted phenotype of natural killer cells in VEXAS syndrome.","authors":"Paul Breillat,Francesco Carbone,Emilie Lereclus,Quentin Riller,Thibaut d'Izarny-Gargas,Celine Posseme,Marie Templé,Lin-Pierre Zhao,Marine Luka,Estibaliz Lazaro,Roderau Outh,Guillaume Le Guenno,Francois Lifermann,Yannick Dieudonné,Marie Berleur,Cédric Lenormand,Karl Balabanian,Thierry Weitten,Vivien Guillotin,Marie Kostine,Barbara Burroni,Adrien Bigot,Alexandra Audemard-Verger,Aldric Manuel,Antoine Dossier,Cécile Golden,Jean-Philippe Martellosio,Benoit Faucher,Benjamin De Sainte Marie,Nadine Magy-Bertrand,Valentin Lacombe,Stéphane Vinzio,Sylvie Grosleron,Léa Dionet,Pierre-Louis Tharaux,Darragh Duffy,Mickaël Mathieu Ménager,Nicolas Dulphy,Olivier Kosmider,Benjamin Terrier","doi":"10.1182/blood.2024028216","DOIUrl":"https://doi.org/10.1182/blood.2024028216","url":null,"abstract":"VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is an autoinflammatory disorder caused by acquired somatic UBA1 mutations in hematopoietic stem cells, affecting peripheral myeloid and natural killer (NK) cells. Given the high rate of severe infections observed in VEXAS patients, we hypothesized that NK cell dysfunction contributes to this increased susceptibility. We conducted a comprehensive immune characterization of peripheral NK cells in patients with VEXAS (n=40), patients with autoinflammatory diseases without UBA1 mutations (n=22), and elderly gender-matched healthy controls (HCs) (n=16). Multiparameter phenotyping was performed using CyTOF, scRNAseq, whole blood stimulation assays and in vitro NK cell cytotoxic assay. Peripheral NK cells in VEXAS were quantitatively and qualitatively impaired. Mass cytometry revealed reduced frequencies of mature cytotoxic CD56dim NK cells and an expansion of the CD56high CD16dim subset. NK cells exhibited features of exhaustion, including increased PD-1 expression, and reduced levels of cytotoxic markers such as NKp46 and CD8α. scRNAseq analysis showed decreased signatures of cytotoxicity and IL-2 and IFN-γ production, alongside increased inflammatory signatures. Whole blood stimulation assays confirmed impaired IL-2, IFN-γ, and granzyme B production following TLR3, TLR4, and TLR7/TLR8 agonist stimulation. Extended NK phenotyping by flow cytometry confirmed reduced activating receptors' expression and impaired IFN-γ production in VEXAS. Moreover, in vitro UBA1 inhibitors impaired NK cell cytotoxic capacity and promote cell death. Finally, reduced NK cell frequencies were independently associated with an increased risk of severe infections. These findings suggest that NK cell dysfunction in VEXAS syndrome contributes to increased susceptibility to severe infections.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"26 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144737358","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}