Blood最新文献_第9页

α-Ketoglutarate dehydrogenase is a therapeutic vulnerability in acute myeloid leukemia

IF 20.3 1区医学

Blood Pub Date : 2024-12-30 DOI: 10.1182/blood.2024025245

Scott E. Millman, Almudena Chaves-Perez, Sudha Janaki-Raman, Yu-Jui Ho, John P. Morris IV, Varun Narendra, Chi-Chao Chen, Benjamin T. Jackson, Jossie J. Yashinskie, Riccardo Mezzadra, Tessa I. Devine, Valentin J. A. Barthet, Michelle Saoi, Timour Baslan, Sha Tian, Zohar Sachs, Lydia W. S. Finley, Justin R. Cross, Scott W. Lowe

{"title":"α-Ketoglutarate dehydrogenase is a therapeutic vulnerability in acute myeloid leukemia","authors":"Scott E. Millman, Almudena Chaves-Perez, Sudha Janaki-Raman, Yu-Jui Ho, John P. Morris IV, Varun Narendra, Chi-Chao Chen, Benjamin T. Jackson, Jossie J. Yashinskie, Riccardo Mezzadra, Tessa I. Devine, Valentin J. A. Barthet, Michelle Saoi, Timour Baslan, Sha Tian, Zohar Sachs, Lydia W. S. Finley, Justin R. Cross, Scott W. Lowe","doi":"10.1182/blood.2024025245","DOIUrl":"https://doi.org/10.1182/blood.2024025245","url":null,"abstract":"Perturbations in intermediary metabolism contribute to the pathogenesis of acute myeloid leukemia (AML) and can produce therapeutically actionable dependencies. Here, we probed whether α-ketoglutarate (αKG) metabolism represents a specific vulnerability in AML. Using functional genomics, metabolomics, and mouse models, we identified the αKG dehydrogenase complex, which catalyzes the conversion of αKG to succinyl CoA, as a molecular dependency across multiple models of adverse-risk AML. Inhibition of 2-oxoglutarate dehydrogenase (OGDH), the E1 subunit of the αKG dehydrogenase complex, impaired AML progression and drove differentiation. Mechanistically, hindrance of αKG flux through the tricarboxylic acid (TCA) cycle resulted in rapid exhaustion of aspartate pools and blockade of de novo nucleotide biosynthesis, whereas cellular bioenergetics was largely preserved. Additionally, increased αKG levels after OGDH inhibition affected the biosynthesis of other critical amino acids. Thus, this work has identified a previously undescribed, functional link between certain TCA cycle components and nucleotide biosynthesis enzymes across AML. This metabolic node may serve as a cancer-specific vulnerability, amenable to therapeutic targeting in AML and perhaps in other cancers with similar metabolic wiring.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"1 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142939870","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}

引用次数: 0

Targeting Enterobacter cloacae attenuates osteolysis by reducing ammonium in multiple myeloma.

IF 21 1区医学

Blood Pub Date : 2024-12-30 DOI: 10.1182/blood.2024025694

Qin Yang, Yinghong Zhu, Xingxing Jian, Yi Qiu, Yan Zhu, Lia Zhao, Yanjuan He, Gang An, Lugui Qiu, Jiaojiao Guo, Nihan He, Huerxidan Abudumijiti, Cong Hu, Xun Chen, Siqing Huang, Xiangling Feng, Xin Li, Jing Liu, Yajing Xu, Wen Zhou

{"title":"Targeting Enterobacter cloacae attenuates osteolysis by reducing ammonium in multiple myeloma.","authors":"Qin Yang, Yinghong Zhu, Xingxing Jian, Yi Qiu, Yan Zhu, Lia Zhao, Yanjuan He, Gang An, Lugui Qiu, Jiaojiao Guo, Nihan He, Huerxidan Abudumijiti, Cong Hu, Xun Chen, Siqing Huang, Xiangling Feng, Xin Li, Jing Liu, Yajing Xu, Wen Zhou","doi":"10.1182/blood.2024025694","DOIUrl":"https://doi.org/10.1182/blood.2024025694","url":null,"abstract":"Multiple myeloma (MM)-induced bone disease affects not only patients' quality of life but also their overall survival. Our previous work demonstrated that the gut microbiome plays a crucial role in MM progression and drug resistance. However, the role of altered gut microbiota in MM bone disease remains unclear. In this study, we show that intestinal E. cloacae is significantly enriched in MM patients with osteolysis. Through fecal microbial transplantation and single bacterial colonization experiments in a 5TGM1 MM mouse model, we found that intestinal colonization of E. cloacae promotes osteolysis by increasing circulating ammonium levels. Elevated ammonium promotes osteoclastogenesis by increasing Trap protein levels in osteoclast precursors and by acetylating and stabilizing CCL3 protein in MM cells. Inhibition of ammonium synthesis, using E. cloacae with a deleted dcd gene, along with probiotic supplementation, alleviated osteolysis in MM. Overall, our work suggests that E. cloacae promotes osteolysis in MM by synthesizing ammonium. This establishes a novel mechanism and potential intervention strategy for managing MM with osteolysis.","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142944568","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}

引用次数: 0

How I Diagnose and Treat Acute Infection-associated Purpura Fulminans.

IF 21 1区医学

Blood Pub Date : 2024-12-30 DOI: 10.1182/blood.2024025078

Pavan K Bendapudi, Julie-Aurore Losman

{"title":"How I Diagnose and Treat Acute Infection-associated Purpura Fulminans.","authors":"Pavan K Bendapudi, Julie-Aurore Losman","doi":"10.1182/blood.2024025078","DOIUrl":"https://doi.org/10.1182/blood.2024025078","url":null,"abstract":"Purpura fulminans (PF) is a rare but devastating complication of sepsis characterized by a highly thrombotic subtype of disseminated intravascular coagulation (DIC). A medical emergency, PF cases often require the involvement of consultant hematologists to assist with diagnosis and management of patients who are in a highly dynamic and deteriorating clinical situation. Patients who survive past the first 24 to 72 hours often die from complications of unchecked thrombosis rather than from shock, and survivors are usually left with severe scarring and tissue loss. Despite these challenging features, PF is a pathophysiologically distinct, homogenous, and highly predictable form of sepsis-associated DIC for which poor outcomes are not a foregone conclusion. The fundamental pathologic lesion in PF is a failure of the anticoagulant protein C pathway, which leads to uncontrolled microvascular clotting and inadequate protein C-mediated cytoprotective effects, which are vital for survival in sepsis. Herein, we review the clinical features and diagnosis of PF. Drawing from the existing clinical literature and from recent advances in our understanding of the pathophysiology of PF, we describe rationally-designed treatment approaches for this disorder, including repletion of natural circulating anticoagulants, use of therapeutic anticoagulation, and ways to optimize transfusion support, and we outline specific interventions that we would recommend avoiding.","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142944639","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}

引用次数: 0

Genetic subtypes of B-cell acute lymphoblastic leukemia in adults.

IF 21 1区医学

Blood Pub Date : 2024-12-30 DOI: 10.1182/blood.2023022919

Marie Passet, Rathana Kim, Emmanuelle Clappier

{"title":"Genetic subtypes of B-cell acute lymphoblastic leukemia in adults.","authors":"Marie Passet, Rathana Kim, Emmanuelle Clappier","doi":"10.1182/blood.2023022919","DOIUrl":"https://doi.org/10.1182/blood.2023022919","url":null,"abstract":"B-cell acute lymphoblastic leukemia (B-ALL) is a rare malignancy in adults with outcomes remaining poor, especially compared to children. Over the past two decades, extensive whole-genome studies have identified numerous genetic alterations driving leukemia, leading to the recognition of more than 20 distinct subtypes which are closely associated with treatment response and prognosis. In pediatric B-ALL, large correlation studies have made genetic classification a central component of risk-adapted treatment strategies. Notably, genetic subtypes are unevenly distributed according to age, and the spectrum of genetic alterations and their prognostic relevance in adult B-ALL have been less extensively studied, with treatment primarily based on the presence or absence of BCR::ABL1 fusion. This review provides an overview of genetic subtypes in adult B-ALL, including recent biological and clinical insights in well-established subtypes as well as data on newly recognized subtypes. Their relevance for risk classification, disease monitoring and therapeutic management, including in the context of B-cell-directed therapies, is discussed. This review advocates for continuing efforts to further improve our understanding of the biology of adult B-ALL to establish the foundation of future precision medicine in B-ALL.","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142944635","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}

引用次数: 0

Odronextamab monotherapy in R/R DLBCL after progression with CAR T-cell therapy: Primary analysis of the ELM-1 study.

IF 21 1区医学

Blood Pub Date : 2024-12-30 DOI: 10.1182/blood.2024027044

Max S Topp, Matthew J Matasar, John N Allan, Stephen M Ansell, Jeffrey A Barnes, Jon E Arnason, Jean-Marie Michot, Neta Goldschmidt, Susan M O'Brien, Uri Abadi, Irit Avivi, Yuan Cheng, Dina M Flink, Min Zhu, Jurriaan Brouwer-Visser, Aafia Chaudhry, Hesham Mohamed, Srikanth Ambati, Jennifer L Crombie

{"title":"Odronextamab monotherapy in R/R DLBCL after progression with CAR T-cell therapy: Primary analysis of the ELM-1 study.","authors":"Max S Topp, Matthew J Matasar, John N Allan, Stephen M Ansell, Jeffrey A Barnes, Jon E Arnason, Jean-Marie Michot, Neta Goldschmidt, Susan M O'Brien, Uri Abadi, Irit Avivi, Yuan Cheng, Dina M Flink, Min Zhu, Jurriaan Brouwer-Visser, Aafia Chaudhry, Hesham Mohamed, Srikanth Ambati, Jennifer L Crombie","doi":"10.1182/blood.2024027044","DOIUrl":"https://doi.org/10.1182/blood.2024027044","url":null,"abstract":"Patients with relapsed/refractory (R/R) diffuse large B-cell lymphoma (DLBCL) progressing after chimeric antigen receptor T-cell therapy (CAR T) have dismal outcomes. The prespecified post-CAR T expansion cohort of the ELM-1 study investigated the efficacy and safety of odronextamab, a CD20×CD3 bispecific antibody, in patients with disease progression after CAR T. Sixty patients received IV odronextamab weekly for 4 cycles followed by maintenance until progression. The primary endpoint was objective response rate (ORR) by independent central review. The median number of prior lines of therapy was 3 (range 2-9), 71.7% were refractory to CAR T, and 48.3% relapsed within 90 days of CAR T. After a median follow-up of 16.2 months, ORR and complete response (CR) rate were 48.3% and 31.7%, respectively. Responses were similar across prior CAR T products and time to relapse on CAR T. Median duration of response was 14.8 months and median duration of CR was not reached. Median progression-free survival and overall survival were 4.8 months and 10.2 months, respectively. The most common treatment-emergent adverse event was cytokine release syndrome (48.3%; no Grade ≥3 events). No cases of immune effector cell-associated neurotoxicity syndrome were reported. Grade ≥3 infections occurred in 12 patients (20.0%), two of which were COVID-19. Odronextamab monotherapy demonstrated encouraging efficacy and generally manageable safety, supporting its potential as an off-the-shelf option for post-CAR T patients. This trial was registered at www.clinicaltrials.gov as #NCT02290951.","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142944649","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}

引用次数: 0

Targeting WDR5/ATAD2 signaling by the CK2/Ikaros axis demonstrates therapeutic efficacy in T-ALL.

IF 21 1区医学

Blood Pub Date : 2024-12-27 DOI: 10.1182/blood.2024024130

Qi Han, Yan Gu, Huimin Xiang, Linyao Zhang, Yan Wang, Chan Yang, Jun Li, Chelsea Steiner, Rosa Lapalombella, Jennifer A Woyach, Yiping Yang, Sinisa Dovat, Chunhua Song, Zheng Ge

{"title":"Targeting WDR5/ATAD2 signaling by the CK2/Ikaros axis demonstrates therapeutic efficacy in T-ALL.","authors":"Qi Han, Yan Gu, Huimin Xiang, Linyao Zhang, Yan Wang, Chan Yang, Jun Li, Chelsea Steiner, Rosa Lapalombella, Jennifer A Woyach, Yiping Yang, Sinisa Dovat, Chunhua Song, Zheng Ge","doi":"10.1182/blood.2024024130","DOIUrl":"https://doi.org/10.1182/blood.2024024130","url":null,"abstract":"T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with a poor prognosis and limited options for targeted therapies. Identifying new molecular targets to develop novel therapeutic strategies is the pressing immediate issue in T-ALL. Here, we observed high expression of WD Repeat-Containing Protein 5 (WDR5) in T-ALL; with in vitro and in vivo models we demonstrated the oncogenic role of WDR5 in T-ALL by activating cell cycle signaling through its new downstream effector, ATPase family AAA domain-containing 2 (ATAD2). Moreover, IKAROS' function is often impaired by genetic alteration as well as casein kinase II (CK2) which is overexpressed in T-ALL. We found IKAROS directly regulates WDR5 transcription; CK2 inhibitor, CX-4945 strongly suppresses WDR5 expression by restoring IKAROS function. Lastly, combining CX-4945 with WDR5 inhibitor demonstrates synergistic efficacy in the patient-derived xenograft mouse models. In conclusion, our results demonstrated that WDR5/ATAD2 is a new oncogenic signaling pathway in T-ALL, and simultaneous targeting of WRD5 and CK2/IKAROS has synergistic anti-leukemic efficacy and represents a promising potential strategy for T-ALL therapy.","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142944653","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}

引用次数: 0

Novel Treatment Strategies for Chronic Myeloid Leukemia.

IF 20.3 1区医学

Blood Pub Date : 2024-12-27 DOI: 10.1182/blood.2024026312

Nataly Cruz-Rodriguez,Michael W Deininger

{"title":"Novel Treatment Strategies for Chronic Myeloid Leukemia.","authors":"Nataly Cruz-Rodriguez,Michael W Deininger","doi":"10.1182/blood.2024026312","DOIUrl":"https://doi.org/10.1182/blood.2024026312","url":null,"abstract":"Starting with imatinib, tyrosine kinase inhibitors (TKIs) have turned chronic myeloid leukemia (CML) from a lethal blood cancer into a chronic condition. As patients with access to advanced CML care have an almost normal life expectancy, there is a perception that CML is a problem of the past, and one should direct research resources elsewhere. However, a closer look at the current CML landscape reveals a more nuanced picture. Most patients still require life-long TKI therapy to avoid recurrence of active CML. Chronic TKI toxicity and the high costs of the well-tolerated agents remain challenging. Progression to blast phase still occurs, particularly in socioeconomically disadvantaged parts of the world, where high risk CML at diagnosis is common. Here we will review the prospects of further improving TKIs to achieve optimal suppression of BCR::ABL1 kinase activity, the potential of combining different classes of TKIs, and the current state of BCR::ABL1 degraders. We will cover combination therapy approaches to address TKI resistance in the setting of residual leukemia and in advanced CML. Despite the unprecedented success of TKIs in CML, more work is needed to truly finish the job, and we hope to stimulate innovative research aiming to achieve this goal.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"54 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142887459","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}

引用次数: 0

TR4 and BCL11A repress γ-globin transcription via independent mechanisms. TR4和BCL11A通过独立机制抑制γ-球蛋白转录

IF 21 1区医学

Blood Pub Date : 2024-12-26 DOI: 10.1182/blood.2024024599

Yu Wang, Greggory Myers, Lei Yu, Kaiwen Deng, Ginette Balbin-Cuesta, Sharon A Singh, Yuanfang Guan, Rami Khoriaty, James Douglas Engel

{"title":"TR4 and BCL11A repress γ-globin transcription via independent mechanisms.","authors":"Yu Wang, Greggory Myers, Lei Yu, Kaiwen Deng, Ginette Balbin-Cuesta, Sharon A Singh, Yuanfang Guan, Rami Khoriaty, James Douglas Engel","doi":"10.1182/blood.2024024599","DOIUrl":"10.1182/blood.2024024599","url":null,"abstract":"Abstract: Nuclear receptor TR4 (NR2C2) was previously shown to bind to the -117 position of the γ-globin gene promoters in vitro, which overlaps the more recently described BCL11 transcription factor A (BCL11A) binding site. The role of TR4 in human γ-globin gene repression has not been extensively characterized in vivo, whereas any relationship between TR4 and BCL11A regulation through the γ-globin promoters is unclear at present. We show here that TR4 and BCL11A competitively bind in vitro to distinct, overlapping sequences, including positions overlapping -117 of the γ-globin promoter. We found that TR4 represses γ-globin transcription and fetal hemoglobin accumulation in vivo in a BCL11A-independent manner. Finally, examination of the chromatin occupancy of TR4 within the β-globin locus, compared with BCL11A, shows that both bind avidly to the locus control region and other sites, but only BCL11A binds to the γ-globin promoters at statistically significant frequency. These data resolve an important discrepancy in the literature and, thus, clarify possible approaches to the treatment of sickle cell disease and β-thalassaemia.","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"2762-2772"},"PeriodicalIF":21.0,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142406070","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}

引用次数: 0

Deletions in the MAL gene result in loss of Mal protein, defining the rare inherited AnWj-negative blood group phenotype. MAL 基因缺失会导致 Mal 蛋白缺失，从而形成罕见的 AnWj 阴性血型遗传表型。

IF 21 1区医学

Blood Pub Date : 2024-12-26 DOI: 10.1182/blood.2024025099

Louise A Tilley, Vanja Karamatic Crew, Tosti J Mankelow, Samah A AlSubhi, Benjamin Jones, Abigail Borowski, Vered Yahalom, Lilach Finkel, Belinda K Singleton, Piers J Walser, Ashley M Toye, Timothy J Satchwell, Nicole M Thornton

{"title":"Deletions in the MAL gene result in loss of Mal protein, defining the rare inherited AnWj-negative blood group phenotype.","authors":"Louise A Tilley, Vanja Karamatic Crew, Tosti J Mankelow, Samah A AlSubhi, Benjamin Jones, Abigail Borowski, Vered Yahalom, Lilach Finkel, Belinda K Singleton, Piers J Walser, Ashley M Toye, Timothy J Satchwell, Nicole M Thornton","doi":"10.1182/blood.2024025099","DOIUrl":"10.1182/blood.2024025099","url":null,"abstract":"Abstract: The genetic background of the high prevalence red blood cell antigen AnWj has remained unresolved since its identification in 1972, despite reported associations with both CD44 and Smyd1 histone methyltransferase. Development of anti-AnWj, which may be clinically significant, is usually due to transient suppression of antigen expression, but a small number of individuals with persistent, autosomally recessive inherited AnWj-negative phenotype have been reported. Whole-exome sequencing of individuals with the rare inherited AnWj-negative phenotype revealed no shared mutations in CD44H or SMYD1; instead, we discovered homozygosity for the same large exonic deletion in MAL, which was confirmed in additional unrelated AnWj-negative individuals. MAL encodes an integral multipass membrane proteolipid, myelin and lymphocyte protein (Mal), which has been reported to have essential roles in cell transport and membrane stability. AnWj-positive individuals were shown to express full-length Mal on their red cell membranes, which was not present on the membranes of AnWj-negative individuals, regardless of whether from an inherited or suppression background. Furthermore, binding of anti-AnWj was able to inhibit binding of anti-Mal to AnWj-positive red cells, demonstrating the antibodies bind to the same molecule. Overexpression of Mal in an erythroid cell line resulted in the expression of AnWj antigen, regardless of the presence or absence of CD44, demonstrating that Mal is both necessary and sufficient for AnWj expression. Our data resolve the genetic background of the inherited AnWj-negative phenotype, forming the basis of a new blood group system, further reducing the number of remaining unsolved blood group antigens.","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"2735-2747"},"PeriodicalIF":21.0,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141999337","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}

引用次数: 0

Auer rod-like inclusions in B-cell lymphoma mimicking therapy-related acute myeloid leukemia.

IF 20.3 1区医学

Blood Pub Date : 2024-12-26 DOI: 10.1182/blood.2024025759

Elena Frye Naharro,Michael A Linden

引用次数: 0