Blood最新文献

{"title":"Standard-of-care idecabtagene vicleucel for relapsed/refractory multiple myeloma.","authors":"Surbhi Sidana, Nausheen Ahmed, Othman Salim Akhtar, Ruta Brazauskas, Temitope Oloyede, Matthew Bye, Doris Hansen, Christopher Ferreri, Ciara L Freeman, Aimaz Afrough, Larry D Anderson, Binod Dhakal, Devender Dhanda, Lohith Gowda, Hamza Hashmi, Melanie J Harrison, Amani Kitali, Heather Landau, Abu-Sayeef Mirza, Pallavi Patwardhan, Muzaffar Qazilbash, Saad Usmani, Krina Patel, Taiga Nishihori, Siddhartha Ganguly, Marcelo C Pasquini","doi":"10.1182/blood.2024026216","DOIUrl":"10.1182/blood.2024026216","url":null,"abstract":"<p><strong>Abstract: </strong>Idecabtagene vicleucel (ide-cel) was the first US Food and Drug Administration-approved chimeric antigen receptor T-cell (CAR-T) therapy for multiple myeloma (MM). However, because clinical trials are highly selective with stringent eligibility criteria, the objective of this study was to evaluate the safety and effectiveness of standard-of-care (SOC) ide-cel in the real world. Using the Center for International Blood and Marrow Transplant Research registry, we evaluated 821 patients who received SOC ide-cel. Median follow-up was 11.6 months. Median age was 66 years, and the cohort included 31% patients aged ≥70 years, with 15% Black and 7% Hispanic, and 77% of patients with ≥1 significant comorbidity. The median number of prior lines of therapy was 7, 15% patients previously received B-cell maturation antigen-directed therapy, 17% had extramedullary disease, and 27% had high-risk cytogenetics. Overall response rate was 73%, and complete response rate was 25%. Median progression-free survival was 8.8 months. Treatment-related mortality was reported in 6% of patients. Cytokine release syndrome was diagnosed in 80% of patients (grade ≥3, 3%). Immune effector cell-associated neurotoxicity syndrome was observed in 28% (grade ≥3, 5%), with no cases of Parkinsonism reported. Clinically significant infections were seen in 45% of patients. Second primary malignancies were reported in 4%, including 1% myeloid malignancies. This is, to our knowledge, the largest real-world study of ide-cel CAR-T therapy in patients with relapsed/refractory (R/R) MM. We observed a favorable safety and efficacy profile that mirrors trial experience, even in the setting of significant comorbidities in 77% of patients, many of which would have made them ineligible for the registrational KarMMa clinical trial. This trial was registered at www.clinicaltrials.gov as #NCT03361748.</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"167-177"},"PeriodicalIF":21.0,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810464","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":"Unveiling the truth: different names, same antigen.","authors":"Nelson H Tsuno,Daisuke Takahashi","doi":"10.1182/blood.2025028939","DOIUrl":"https://doi.org/10.1182/blood.2025028939","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"34 1","pages":"141-143"},"PeriodicalIF":20.3,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144594036","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":"BRAF V600E-positive mononuclear cells in blood at diagnosis portend treatment failure and neurodegeneration in pediatric LCH.","authors":"Howard Lin, Akanksha Batajoo, Erin Peckham-Gregory, Daniel Zinn, Olive S Eckstein, Nader Kim El-Mallawany, Nitya Gulati, Zachary D Prudowsky, Brooks Scull, Jessica Velazquez, Harshal Abhyankar, Stephen J Simko, Daria Vakula, Ryan Fleischmann, Vivekanudeep Karri, M John Hicks, Kevin E Fisher, Choladda V Curry, Angshumoy Roy, Deborah Schiff, Kenneth M Heym, Michael E Scheurer, D Williams Parsons, Miriam Merad, Tsz-Kwong Man, Kenneth L McClain, Jennifer Picarsic, Carl E Allen","doi":"10.1182/blood.2024026671","DOIUrl":"10.1182/blood.2024026671","url":null,"abstract":"<p><strong>Abstract: </strong>Langerhans cell histiocytosis (LCH) is a myeloid neoplastic disorder driven by mitogen-activated protein kinase (MAPK) activation in hematopoietic cells. Historically, LCH has been staged according to involvement of \"risk organs\" (bone marrow, liver, and spleen), based on risk of death. With improvements in supportive care and efficacy of MAPK pathway inhibitors, patients with LCH now rarely die. However, most patients with LCH with multisystem disease are not cured with current front-line chemotherapy, and treatment failure is associated with long-term morbidity, including LCH-associated neurodegeneration (LCH-ND). In this study, we evaluated the impact of extent of LCH at presentation, tumor genotype, and BRAFV600E in pretherapy peripheral blood mononuclear cells (PBMCs) and bone marrow on systemic and central nervous system outcomes in a cohort of 385 pediatric patients with LCH and 115 adults with LCH, followed up for a median of 4 years (range, 0.02-18 years). Five-year event-free survival was 50.7% for pediatric patients and 32.7% for adult patients with LCH. In the pediatric cohort, presence of BRAFV600E PBMC was strongly associated with front-line treatment failure (hazard ratio [HR], 7.7). Remarkably, BRAFV600E PBMC at diagnosis also identified patients at the highest risk of developing LCH-ND (HR, 23.1). These findings support an updated model of pediatric LCH pathogenesis in which persistence of disease reservoir and cell of origin determine extent of disease and clinical risks. We, therefore, propose a major revision of pediatric LCH diagnostic staging, shifting from focus on historical risk of death to risks of systemic treatment failure and LCH-ND based on lesion location, lesion genotype, and peripheral LCH reservoir (eg, BRAFV600E PBMC).</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"206-218"},"PeriodicalIF":21.0,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751115","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":"Matched donor allogeneic CAR-T for adult B-ALL: toxicity, efficacy, repeat dosing, and the importance of lymphodepletion.","authors":"Claire Roddie,Juliana Dias,Maeve O'Reilly,Mahnaz Abbasian,Amaia Cadinanos-Garai,Ketki Vispute,Leticia Bosshard-Carter,Marina Mitsikakou,Eftychia Charalambous,Vedika Mehra,Harriet Roddy,Gordon Weng-Kit Cheung,John A Hartley,Nasir Galal Mahmoud,Leah Ensell,Yashma Patel,Maria A V Marzolini,Farzin Farzaneh,Lauren Nickolay,Nourredine Himoudi,Farhatullah Syed,Bilyana Popova,Sevasti Galani,Alexander Day,Mark W Lowdell,Karl S Peggs","doi":"10.1182/blood.2025028790","DOIUrl":"https://doi.org/10.1182/blood.2025028790","url":null,"abstract":"Autologous CD19-targeting CAR-T has transformed management of relapsed/refractory adult B-cell acute lymphoblastic leukaemia(B-ALL) but relapse post-allogeneic stem cell transplant(allo-SCT) is frequently accompanied by profound lymphopenia, impaired T-cell fitness and aggressive disease requiring urgent treatment, making autologous CAR-T challenging to deliver. We developed an allogeneic matched-donor CD19CAR product (CAR-DLI) for adult B-ALL following allo-SCT failure. Here we evaluate the risks/benefits of pre-CAR-DLI lymphodepleting chemotherapy (LD), and the efficacy of repeat CAR-DLI dosing as per conventional DLI scheduling/protocols. Patients aged 16-70y with r/r B-ALL post-allo-SCT were eligible. Primary outcomes were toxicity and feasibility of CAR-DLI manufacture; secondary outcomes included CAR-DLI engraftment/ expansion/ persistence. 17 allo-SCT donors were leukapheresed and 14 patients (median age,43y) were infused. Median disease burden at registration was 63.5% bone marrow blasts (range, MRD-100%). Patients 1-7 received CAR-DLI-alone; patients 8-14 received CAR-DLI+LD with fludarabine/cyclophosphamide. CAR-DLI+LD vs CAR-DLI-alone was associated with superior peak CAR-DLI engraftment (93,134 vs. 8010 copies/ug gDNA), expansion (858,101 vs. 39,038 copies/ug gDNA/28d) and persistence (median 197 days vs. 32 days). CAR-DLI+LD was not associated with more immunotoxicity than CAR-DLI-alone, and GvHD (grade-1/skin) affected only 2/14(14%) patients. CAR-DLI+LD vs CAR-DLI-alone conferred superior event-free-survival (EFS) and overall-survival (OS) at 12m (57% vs 29%; 83% vs 29%). Repeat CAR-DLI dosing was administered to 8/14(57%) patients with morphological/MRD+ relapse, but with minimal engraftment/expansion or toxicity/efficacy. CAR-DLI+LD has a tolerable safety profile without significant GvHD and is associated with significantly better outcomes than CAR-DLI-alone. Repeat CAR-DLI dosing beyond dose 1 was not found to be effective in this analysis. NCT02893189.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"4 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144603957","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":"Structure and interactions of the proteins from the contact system.","authors":"Jonas Emsley,Yujie Ma,Joost C M Meijers","doi":"10.1182/blood.2024025322","DOIUrl":"https://doi.org/10.1182/blood.2024025322","url":null,"abstract":"The contact system includes factor XII (FXII), factor XI (FXI), prekallikrein (PK) and high-molecular weight kininogen (HK) and has received increased interest as a potential target in immunothrombotic and inflammatory diseases. This system activates two distinct pathways, the intrinsic pathway of coagulation via cleavage of factor IX (FIX) and inflammation via HK cleavage resulting in bradykinin (BK) generation. HK is central to the function of both arms of the system as a substrate for plasma kallikrein (PKa) and critical cofactor which forms interactions with cell receptors and activators. Both FXI and PK circulate in complex with HK and both can be activated by factor XIIa (FXIIa). Reciprocal activation and continuous consumption of PK and FXII is a feature of the contact system. On endothelial cells, PK and FXII become activated but only in the presence of secreted receptor for the globular domain of C1q (gC1qR) and Zn2+ ions. A second mechanism exists on endothelial cells whereby prolylcarboxypeptidase activates the PK-HK complex to generate BK in a FXII independent manner. On platelets, FXI can be cleaved by thrombin, but only in the presence of secreted polyphosphate. This review explores the 3D structure of the contact factors and examines the molecular mechanisms underlying contact activation. We focus on conformational changes that expose cleavage sites and exosites in FXII, PK, and FXI. We also discuss contact factor protein-protein interactions, recognition of polyanions and the role of HK and Zn²⁺ in contact system assembly.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"93 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144603964","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":"Immune Alterations in Myeloma Evolution and Outcomes: Quo Vadis?","authors":"Madhav V Dhodapkar,Bruno Paiva","doi":"10.1182/blood.2024026227","DOIUrl":"https://doi.org/10.1182/blood.2024026227","url":null,"abstract":"The pathogenesis of multiple myeloma (MM) and its precursor monoclonal gammopathy of undetermined significance (MGUS) is linked to an aging immune system. Chronic activation of B/plasma cells may contribute to the origin of MGUS, which is frequent in the elderly. However, only 1% of individuals with MGUS annually experience progression to MM. The immune system can specifically recognize MGUS lesions and preclinical MM models provide evidence for both innate and adaptive immune surveillance. Multiomic studies have identified several systemic alterations at the MGUS stage, suggesting accelerated immune aging prior to evolution into clinical malignancy. MM is further associated with spatial alterations in patterns of tumor growth and in-situ regulation of regional immunity. Both tumor and microenvironment-related factors contribute to immune paresis, which facilitates the dissemination of clonal plasma cells and increases the risk of infections in MM patients. Immune profiles in blood or marrow exhibit considerable heterogeneity and have been linked to outcomes following immune therapies including T cell redirection. Understanding how underlying systemic immune changes impact in-vivo function and durability of natural or synthetic tumor/antigen-specific immunity needs further study. Preserving or restoring immune function may be critical for long-term outcomes both in the context of prevention of clinical MM and of treating active disease. Benchmarking of immune biomarkers followed by its prospective integration into current risk models, together with improved understanding of mechanisms underlying tumor immunity in-vivo, are needed to optimize immune approaches and improve outcomes in MM.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"9 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144578665","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":"Outcomes of Allogeneic HCT in Hodgkin Lymphoma in the Era of Checkpoint Inhibitors: A Joint CIBMTR and EBMT Analysis.","authors":"Miguel-Angel Perales,Farrukh T Awan,Ariane Boumendil,Jinalben Patel,Luca Castagna,Emanuele Angelucci,Herve Finel,Alexander D Kulagin,Bertram Glass,Paolo Corradini,Alex F Herrera,Didier Blaise,Mohamed A Kharfan-Dabaja,Khalid Halahleh,Sairah Ahmed,Carmen Martinez,Sebastian Giebel,Silvia Montoto,Richard J Jones,Nausheen Ahmed,Ryan C Lynch,Marcos J de Lima,Mazyar Shadman,Craig S Sauter,Kwang Woo Ahn,Mehdi Hamadani,Ali Bazarbachi,Anna Sureda","doi":"10.1182/blood.2024027197","DOIUrl":"https://doi.org/10.1182/blood.2024027197","url":null,"abstract":"Checkpoint inhibitors (CPI) have shown remarkable efficacy in patients with Hodgkin lymphoma (HL) and are now used routinely for this disease. While allogeneic hematopoietic cell transplantation (alloHCT) remains a curative option for HL, there are concerns that prior CPI may exacerbate post alloHCT complications, particularly graft-versus-host disease (GVHD), and lead to worse outcomes. Given the relative paucity of data, we performed a CIBMTR/EBMT study to examine the impact of prior CPI in alloHCT outcomes. We included 2186 adult patients > 18 years who received a first alloHCT using a matched related, unrelated or haploidentical donor from 2008-2023. Twenty-seven percent of patients received prior CPI. GVHD prophylaxis was post-transplant cyclophosphamide in 55.8% patients in the CPI cohort and 35% in the non-CPI cohort. Median follow-up among survivors was longer for the non-CPI (39 months) than CPI cohort (16.5 months). In the multivariate analysis, prior CPI exposure did not affect overall survival or non-relapse mortality but resulted in improved progression-free survival (non-CPI vs. CPI HR 0.81, 0.67-0.98, p=0.03) and lower incidence of relapse (HR 0.58, 0.45-0.76, p<0001). While grade II-IV (HR1.26, 1.04-1.53; p=0.02) and III-IV (HR1.41, 1.04-1.92; p=0.03) acute GVHD were increased differences in chronic GVHD were not significant. Use of post-transplant cyclophosphamide based GVHD prophylaxis resulted in improved OS, lower grade II-IV acute GVHD and chronic GVHD in patients with prior CPI exposure. In summary, allo-HCT should still be considered a curative option for patients with HL in the era of checkpoint inhibitors.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"106 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144578664","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":"IFN-γ promotes the progression of iMCD by activating inflammatory monocytes.","authors":"Xuejiao Yin, Yi Liu, Shengnan Ding, Jiaying Ge, Min Yang, Zhenbo Wang, Zuopo Lv, Xuxia Luo, Liya Ma, Wenjuan Yu, Juying Wei, Chunmei Yang, Qiumei Yao, Li Zhu, Shuqi Zhao, Yu Chen, Haitao Meng, Jie Jin, Hongyan Tong, Liangshun You","doi":"10.1182/blood.2024027689","DOIUrl":"10.1182/blood.2024027689","url":null,"abstract":"<p><strong>Abstract: </strong>A deeper understanding of the immune landscape in patients with idiopathic multicentric Castleman disease (iMCD) is essential to establish early prognostic stratification and uncover novel therapeutic targets. We used single-cell RNA sequencing of peripheral blood mononuclear cells (PBMCs) from a cohort of 15 patients with iMCD and 4 healthy controls. To explore the sources of interleukin-6 (IL-6), we included lymph node and bone marrow samples for comparison with PBMCs. Our results indicate that IL-6 primarily originates from the lymph nodes, particularly from activated B cells. Similarly, in peripheral blood, activated B cells are also the main source of IL-6. IL-6 receptor is primarily expressed in monocytes in PBMCs, with CCL monocytes showing the strongest activation of the IL-6 signaling pathway. This suggests that CCL monocytes in iMCD may play an important role in driving peripheral inflammatory storms. CellChat analysis reveals that during disease flares, CCL monocytes interact with specific natural killer (NK)/NKT cells through enhanced type II interferon (IFN-II) signaling, whereas this interaction significantly diminishes during remission, indicating a significant role for IFN-II in the pathogenesis of iMCD. Notably, serum IFN-γ levels positively correlate with both disease severity and treatment resistance, a finding validated by a large independent iMCD cohort. Our findings confirm that the IL-6 pathway remains central to iMCD pathogenesis and highlight a significant role for IFN-II pathway activation in amplifying inflammatory storms. Our findings provide valuable biomarkers for assessing disease severity and identify new therapeutic targets for iMCD.</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"76-88"},"PeriodicalIF":21.0,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751129","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 novel mouse model of hemoglobin SC disease reveals mechanisms underlying beneficial effects of hydroxyurea.","authors":"Tahereh Setayesh, Mengna Chi, Zachery Oestreicher, Masahide Sakabe, Katie Seu, Zhenqi Zhu, Harsimran Kaur, Anifat Tijani, Mei Xin, Amy Shova, Kenneth D Greis, Tim M Townes, József Balla, Katherine VandenHeuvel, Yueh-Chiang Hu, Punam Malik","doi":"10.1182/blood.2024028136","DOIUrl":"10.1182/blood.2024028136","url":null,"abstract":"<p><strong>Abstract: </strong>Sickle cell hemoglobin C (HbSC) disease results from compound heterozygosity of hemoglobin S (HbS) and hemoglobin C (HbC), comprising 30% of sickle cell disease (SCD). HbC induces red blood cell (RBC) dehydration/xerocytosis, which promotes sickling. HbSC-SCD causes significant morbidity despite being milder than homozygous HbSS-SCD. Current research/treatment strategies have focused on HbSS-SCD, whereas patients with HbSC are deprived of disease-modifying/transformative therapies because of lack of preclinical models. We generated HbSC mice, which resemble human HbSC-SCD: HbSC erythrocytes showed marked xerocytosis. Anemia, hemolysis, inflammation, and organ damage were milder than HbSS mice but hypoxia/reperfusion injury was similar. Retinopathy developed at higher frequency than HbSS mice (66.7% vs 16.7%; P < .05), as in patients with HbSC-SCD. Although HbSC RBCs sickled at lower oxygen tension than HbSS RBCs, they did not completely recover deformability after hypoxia/reoxygenation. Using the HbSC mice, we studied the mechanism by which hydroxyurea causes significant clinical benefit in patients with HbSC-SCD, despite minimal/modest increases in fetal Hb (HbF). We found hydroxyurea had distinct non-HbF and HbF effects. Hydroxyurea did not increase HbF in adult HbSC/HbSS mice but reduced RBC reactive oxygen species, ferryl Hb, and Heinz-body formation, thereby reducing membrane damage; however, RBC hydration was unaffected. When given to unborn pups before γ-globin expression was switched off, and continued postnatally, we could induce HbF in both HbSC and HbSS mice (higher HbF in HbSS vs HbSC mice). Minimal increases in HbF (∼1%) improved HbSC RBC hydration. Peak HbF levels of 7% in HbSC mice abrogated sickling. Overall, this HbSC model will help bridge the knowledge gap in mechanistic/therapeutic studies in this neglected disease.</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"13-28"},"PeriodicalIF":21.0,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963693","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":"Another 1q bites the dust.","authors":"Vikas A Gupta, Lawrence H Boise","doi":"10.1182/blood.2025028903","DOIUrl":"https://doi.org/10.1182/blood.2025028903","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"146 1","pages":"7-8"},"PeriodicalIF":21.0,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552169","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}