Blood最新文献

{"title":"Unlocking myeloma's spatial world at the micrometer scale.","authors":"Leo Rasche,Niels Weinhold","doi":"10.1182/blood.2025030205","DOIUrl":"https://doi.org/10.1182/blood.2025030205","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"128 1","pages":"1744-1746"},"PeriodicalIF":20.3,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246876","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":"Smarter combos, stronger T cells in lymphoma.","authors":"Santosha A Vardhana","doi":"10.1182/blood.2025030331","DOIUrl":"https://doi.org/10.1182/blood.2025030331","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"26 1","pages":"1742-1744"},"PeriodicalIF":20.3,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246878","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":"Introduction to a review series on follicular lymphoma: solved or insoluble problem?","authors":"Philippe Armand","doi":"10.1182/blood.2025030824","DOIUrl":"https://doi.org/10.1182/blood.2025030824","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"35 1","pages":"1739-1740"},"PeriodicalIF":20.3,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246904","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":"Mel200 or BuMel conditioning in myeloma: is there a winner?","authors":"Donna E Reece","doi":"10.1182/blood.2025030399","DOIUrl":"https://doi.org/10.1182/blood.2025030399","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"82 1","pages":"1741-1742"},"PeriodicalIF":20.3,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246877","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":"Distinct Biological Subtypes of Chronic GVHD after Pediatric Hematopoietic Cell Transplantation.","authors":"Bernard Ng,Andrew C Harris,Sayeh Abdossamadi,Geraldine Aubert,Rajinder P Bajwa,Monica Bhatia,Henrique Bittencourt,Nataliya Prokopenko Buxbaum,Emi H Caywood,Sonali Chaudhury,Joseph H Chewning,Sung Won Choi,Ashley Chopek,Julia Chu,Donald Coulter,Shahinaz M Gadalla,Richard T Hogg,David A Jacobsohn,Amanda K Johnson,Michael Joyce,Kimberly A Kasow,Michael Kent,Carrie L Kitko,Donna Lau,Anita Lawitschka,Victor Anthony Lewis,Amanda M Li,Laura Michelle McLaughlin,David Mitchell,Eneida R Nemecek,Vaishnavi Parthasarathy,Anna B Pawlowska,Filip Pirsl,Michael A Pulsipher,Muna Qayed,Jacob Rozmus,Süreyya Savaşan,Tal Schechter,Shalini Shenoy,Alima Suleimenova,Dong Jun Zheng,Elena Ostroumov,Andrew Gilman,Ramon I Klein Geltink,Daniel Wolff,Geoffrey D E Cuvelier,Kirk R Schultz","doi":"10.1182/blood.2025028625","DOIUrl":"https://doi.org/10.1182/blood.2025028625","url":null,"abstract":"Chronic graft-versus-host-disease (cGvHD) is the primary non-relapse limitation to a successful hematopoietic cell transplantation (HCT) and is largely treated as a single biological entity. We hypothesized that there exist different biological subtypes of cGvHD. Using the ABLE network database, derived from the largest pediatric cGvHD cohort worldwide, we applied clustering analysis to subtype cGvHD patients from the ABLE1.0 and 2.0 studies (51 cGvHD patients, 158 non-cGvHD patients). We found three distinct cGvHD subtypes: cGvHD-1 was characterized by an effector memory (TEM), cytotoxic NK cell, and early precursor B cell predominant pattern; cGvHD-2 was phosphatidylcholine, cytokine, and plasma cells predominant; and cGvHD-3 had more naïve CD4+ T cell (TN) and naïve Treg, had later onset, and the only subtype with measurable TREC. We partially replicated these subtypes using metabolomic data from a separate pediatric cohort of the COG trial ASCT0031 (33 cGvHD patients, 39 non-cGvHD patients). Further, cGvHD-1 was associated with serotherapy (predominantly ATG) exposure, and cGvHD-3 was associated with receiving peripheral blood stem cells (PBSC) from donors, total body irradiation (TBI), and no previous acute GvHD. cGvHD-2 was associated with liver involvement and cGvHD-2 and -3 with de novo cGvHD. Overall, none of the subtypes closely associated with organ involvement. Contrasting each subtype against non-cGvHD patients, the 3 subtypes shared common markers, all of which were used in our previous cGvHD diagnostic classifier. These findings suggest the presence of distinct biological subtypes of cGvHD that may help guide therapeutic strategies.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"8 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246416","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":"Circulating tumor cells predict myeloma outcomes in patients treated with daratumumab, bortezomib, lenalidomide, and dexamethasone.","authors":"Luca Bertamini,Cathelijne Fokkema,Paula Rodriguez-Otero,Mark van Duin,Evangelos Terpos,Mattia D'Agostino,Vincent H J van der Velden,Niels W C J van de Donk,Michel Delforge,Christoph Driessen,Roman Hajek,Hermann Einsele,Annette Juul Vangsted,Diego Vieyra,Ricardo M Attar,Anna Sitthi-Amorn,Robin Carson,Fredrik Schjesvold,Pawel Robak,Meral Beksac,Andrew Spencer,Annemiek Broijl,Tom Cupedo,Philippe Moreau,Mario Boccadoro,Pieter Sonneveld","doi":"10.1182/blood.2025030113","DOIUrl":"https://doi.org/10.1182/blood.2025030113","url":null,"abstract":"Circulating tumor cells (CTC) represent a high-risk biomarker in newly diagnosed multiple myeloma (NDMM); however, their prognostic value among transplant-eligible (TE) patients receiving daratumumab with bortezomib/lenalidomide/dexamethasone (D-VRd) remains unknown. Here, we analyzed CTC in the phase 3 PERSEUS trial (EMN017/NCT03710603). TE patients with NDMM were randomized (1:1) to D-VRd with daratumumab/lenalidomide maintenance (D-VRd group) or VRd with lenalidomide maintenance (VRd group), both with transplant. A subset of 451/709 patients from PERSEUS (D-VRd, 231/355; VRd, 220/354) had screening blood samples collected for CTC analysis by flow cytometry (median follow-up, 47.6 months). CTC were detected in 370/451 (82%) patients (median limit of detection, 0.0004%). CTC were prognostic of progression-free survival (PFS), independently of other factors, as a continuous (HR, 1.36 [95% CI, 1.15-1.60]; P<0.001) and categorical variable (≥0.175% CTC-high, optimal threshold). D-VRd improved PFS versus VRd in CTC-low patients (4-year rates: 88% vs 74%; HR, 0.42 [95% CI, 0.25-0.70]; P=0.0013). Regardless of study treatment, minimal residual disease (MRD)-negativity rates were lower in CTC-high versus CTC-low patients (10-5: 52.2% vs 66.2%; 10-6: 34.8% vs 52.4%). D-VRd significantly increased MRD-negativity rates versus VRd among CTC-high (10-5: 69.4% vs 33.3%; 10-6: 47.2% vs 21.2%; both P<0.05) and CTC-low patients (10-5: 74.4% vs 57.8%; 10-6: 65.6% vs 38.5%; both P<0.001), with similar observations for sustained MRD negativity. CTC levels are an independent prognostic factor in TE-NDMM patients treated with standard-of-care frontline quadruplet. D-VRd improved overall and sustained MRD-negativity rates in CTC-high and CTC-low patients, and improved PFS for CTC-low with a positive trend in CTC-high patients. NCT03710603.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"33 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246417","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 2 trial of rituximab with either pentostatin or bendamustine for multiply relapsed or refractory hairy cell leukemia.","authors":"Brett Schroeder,Constance M Yuan,Hao-Wei Wang,Chirayu Mohindroo,Hong Zhou,Mark Raffeld,Liqiang Xi,Evgeny Arons,Julie Catherine Feurtado,Lacey James-Echenique,Katherine R Calvo,Irina Maric,Robert J Kreitman","doi":"10.1182/blood.2025031243","DOIUrl":"https://doi.org/10.1182/blood.2025031243","url":null,"abstract":"The primary objective in multiply-relapsed hairy cell leukemia and variant (HCL/HCLv) was to determine if pentostatin-rituximab (DCFR) and bendamustine-rituximab (BR) each have overall response rate (ORR) exceeding that historically achieved by rituximab alone (~40%) in favor of 65%. Prospective data was unreported for either regimen. Fifty-six patients received six 28-day cycles of rituximab (375 mg/m² days 1, 15) with either bendamustine (90 mg/m² days 1, 2) or pentostatin (4 mg/m² days 1, 15). Eligibility required ≥2 purine analogs, or one plus rituximab for initial response <1 year. Complete remission (CR) and minimal residual disease (MRD) were studied, and progression-free survival (PFS) with hazard ratios (HR) determined. Although patients were assigned to either regimen through randomization for increasing homogeneity of the two treatment groups, the DCFR arm had fewer prior purine analogs (p=0.021) and lower baseline marrow HCL/HCLv infiltration (p=0.013). ORRs for DCFR and BR were 93% and 86%, 95% confidence intervals (95%CI) 83-102% and 73-99%, each exceeding the primary objective (40% in favor of 65%, p<0.0001 for each). Rates for CR and MRD-free CR and median PFS (141 vs 50 months, HR 0.63, 95%CI 0.32-1.25) numerically favored DCFR but that arm was significantly enriched with lower prior purine analogs and marrow infiltration each of which was associated post hoc with better response. Post hoc subgroup analysis particularly for the 41 patients with classic HCL suggested any superiority of DCFR vs BR might apply to the more favorable patients. DCFR and BR were highly effective in multiply relapsed HCL/HCLv. Possible DCFR superiority was hypothesis-generating, given uneven baseline risks and trial design. NCT01059786.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"23 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246544","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":"Clinical and Research Methods for Analysis and Study of Platelet Populations.","authors":"Thomas Thiele,Johan W M Heemskerk,Andrew L Frelinger","doi":"10.1182/blood.2025028956","DOIUrl":"https://doi.org/10.1182/blood.2025028956","url":null,"abstract":"Blood platelets are crucial in hemostasis, thrombosis and thrombo-inflammation. Current evidence highlights the considerable heterogeneity within subjects in platelet structure, age, and activation properties. This heterogeneity has major implications for the diverse functions of platelets in physiology and pathophysiology extending to therapeutic targeting in hemostasis and cancer. In this review we provide a general concept of heterogeneity or diversity of platelet populations with emphasis on the diagnostic and advanced methodologies to assess and study differences between platelets. We describe conventional and novel approaches to address clinical and in research questions addressing platelet heterogeneity and discuss strengths and limitations of the available techniques.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"21 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145235743","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":"STK10 regulates platelet function in arterial thrombosis and thromboinflammation.","authors":"Yingying Li,Hui Zhu,Yun Liu,Xiaoqian Li,Xiaoyue Zu,Chenyue Wang,Xiaoqi Xu,Yueyue Sun,Yue Dai,Jie Zhang,Shuang Chen,Huimin Jiang,Zhenyu Li,Lingyu Zeng,Kailin Xu,Jianlin Qiao","doi":"10.1182/blood.2025030134","DOIUrl":"https://doi.org/10.1182/blood.2025030134","url":null,"abstract":"Serine-threonine kinase 10 (STK10) is a member of Ste20 family of serine/threonine kinases and regulates lymphocyte adhesion. Quantitative phosphoproteomic assay showed increased STK10 phosphorylation in activated platelet. However, its role in platelet function remains unclear. In our study, we investigated the expression and role of STK10 in platelet function. We first showed STK10 expression in human and mouse platelets. By establishing megakaryocyte/platelet-specific STK10 knockout mice, we found that deletion of platelet STK10 impaired hemostasis and arterial thrombosis. Consistently, platelet aggregation, a-granule release, aIIbb3 activation, procoagulant activity, spreading and clot retraction were all reduced after deletion of STK10. Quantitative phosphoproteomic assays revealed several dysregulated phosphoproteins, which were enriched in platelet activation and focal adhesion. By using immunoprecipitation coupled to mass spectrometry and protein phosphorylation profiles screening approaches, we identified that STK10 interacts with integrin-linked protein kinase (ILK) and deletion of STK10 significantly reduced ILK phosphorylation (Ser343). Following in vitro phosphorylation assay demonstrated that STK10 directly phosphorylated ILK at Ser343. Additionally, inhibition of calcium, PKC or PI3K inhibited STK10 phosphorylation in activated platelets. Moreover, deletion of platelet STK10 reduced platelet-neutrophil interactions, neutrophil accumulation and neutrophil extracellular traps formation, ameliorated thromboinflammation, as well as increased the survival of sepsis mice. Furthermore, an increase of the activation of platelet STK10 and ILK was observed in sepsis mice and patients. In conclusion, our study identifies a novel regulatory role of STK10 in platelet function, arterial thrombosis and thromboinflammation, implying that it might be a potential target for the treatment of thrombotic or cardiovascular diseases.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"81 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145235744","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 Notch trans-activation to cis-inhibition switch underlies hematopoietic stem cell aging.","authors":"Francesca Matteini,Roshana Thambyrajah,Sara Montserrat-Vazquez,Sascha Jung,Alba Ferrer-Perez,Patricia Herrero Molinero,Dina El Jaramany,Javier Lozano-Bartolomé,Eva Mejia-Ramirez,Jessica Gonzalez Miranda,Antonio Del Sol,Anna Bigas,Maria Carolina Florian","doi":"10.1182/blood.2024026505","DOIUrl":"https://doi.org/10.1182/blood.2024026505","url":null,"abstract":"Aged hematopoietic stem cells (HSCs) expand in clusters over time, while reducing their regenerative capacity and their ability to preserve the homeostasis of the hematopoietic system. The expression of Notch ligands in the bone marrow (BM) niche is essential for hematopoiesis. However, the impact of Notch signaling for adult HSC function and its involvement in HSC aging remains controversial. Here we show that Notch activation in young HSCs is not homogeneous, and it is triggered by sinusoidal expression of the Notch ligand Jagged2 (Jag2). Sinusoidal Jag2 deletion in young mice recapitulates the decrease in Notch activity observed in aged HSCs and alters HSC divisional symmetry and fate priming, promoting myeloid-biased HSCs (My-HSCs) expansion. Mechanistically, our data reveals that upon decreasing sinusoidal Jag2 expression, HSCs themselves upregulate Jag2, which cis-inhibits Notch signaling, resulting in the expansion of My-HSCs and in reduced hematopoietic regeneration. Collectively, these findings identify the crosstalk between BM niche-driven and HSC intrinsic features in regulating HSC fate priming and regenerative potential and reveal an extrinsic Notch trans-activation to intrinsic cis-inhibition switch underlying HSC aging.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"26 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145241103","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}