IF 20.3 1区医学

Blood Pub Date : 2025-04-21 DOI: 10.1182/blood.2024026936

Fangwu Wang,Laura Gonzalez,Qiuyu Lian,Colin A Hammond,Yasmine Y M Lau,Benjamin D Simons,Martin Hirst,Connie J Eaves

{"title":"Coordinated regulation of self-renewal and cell cycle during human lympho-myeloid lineage restriction.","authors":"Fangwu Wang,Laura Gonzalez,Qiuyu Lian,Colin A Hammond,Yasmine Y M Lau,Benjamin D Simons,Martin Hirst,Connie J Eaves","doi":"10.1182/blood.2024026936","DOIUrl":"https://doi.org/10.1182/blood.2024026936","url":null,"abstract":"Recent studies indicate the human lympho-myeloid restriction process to be a different and more heterogeneous one than historically inferred. Here we describe the development of bulk and clonal culture systems that efficiently support early B-lymphoid differentiation and its use to elucidate the biological and molecular changes that accompany their initial restriction from subsets of CD34+ human cord blood cells with lympho-myeloid-limited potential. Analyses of these changes revealed that the acquisition of B-lymphoid- and neutrophil/monocyte (NM)-restricted properties are accompanied by a concomitantly accelerated and lineage-shared cell cycling activity and loss of self-renewal potential. Single-cell transcriptome analysis identified reduced expression of multiple self-renewal-associated genes and an accompanying heterogeneous activation of lineage-regulatory modules during the production of B, NM and dendritic cell precursors. By applying a novel culture system that supports early human lymphoid differentiation, we uncover a shared mechanism of proliferation control, along with persistent biological and transcriptional heterogeneity in cells undergoing B and NM lineage restriction.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"37 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143862025","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

Introduction to a How I Treat series on myeloproliferative neoplasms.

IF 20.3 1区医学

Blood Pub Date : 2025-04-17 DOI: 10.1182/blood.2025028401

Jason Gotlib

引用次数: 0

The decline of transplant for relapsed myeloma.

IF 20.3 1区医学

Blood Pub Date : 2025-04-17 DOI: 10.1182/blood.2024028275

Aurore Perrot,Cyrille Touzeau

引用次数: 0

Dual targeting of EZH2 and DOT1L in DLBCL.

IF 20.3 1区医学

Blood Pub Date : 2025-04-17 DOI: 10.1182/blood.2024027324

Jerome Moreaux

引用次数: 0

Can less differentiation drive CARs to success?

IF 20.3 1区医学

Blood Pub Date : 2025-04-17 DOI: 10.1182/blood.2024028274

Natalie S Grover,Barbara Savoldo

引用次数: 0

A rare case of nodal hairy cell leukemia exhibiting characteristic morphological and immunohistochemical features.

IF 20.3 1区医学

Blood Pub Date : 2025-04-17 DOI: 10.1182/blood.2024028020

Soma Roy Chakraborty,Jeremiah X Karrs

引用次数: 0

Early T-precursor acute lymphoblastic leukemia with mature plasmacytoid dendritic cell proliferation.

IF 20.3 1区医学

Blood Pub Date : 2025-04-17 DOI: 10.1182/blood.2024028302

Benjamin Podvin,Adélaïde Hardeman

引用次数: 0

Genotype-specific immune responses at the intestinal barrier predispose to colitis in chronic granulomatous disease in mice.

IF 20.3 1区医学

Blood Pub Date : 2025-04-16 DOI: 10.1182/blood.2024026332

Emma Darbinian,Kodjovi D Mlaga,Prabha Chandrasekaran,Yu Han,Agnes Donkó,Aléhandra Desjardins,Thomas L Leto,Steven M Holland,Johanne Poudrier,Emilia Liana Falcone

{"title":"Genotype-specific immune responses at the intestinal barrier predispose to colitis in chronic granulomatous disease in mice.","authors":"Emma Darbinian,Kodjovi D Mlaga,Prabha Chandrasekaran,Yu Han,Agnes Donkó,Aléhandra Desjardins,Thomas L Leto,Steven M Holland,Johanne Poudrier,Emilia Liana Falcone","doi":"10.1182/blood.2024026332","DOIUrl":"https://doi.org/10.1182/blood.2024026332","url":null,"abstract":"Chronic granulomatous disease (CGD) is an inborn error of immunity caused by defects in any one of the 6 subunits (gp91phox, p47phox, p22phox, p67phox, p40phox or chaperone EROS) forming the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex 2 (NOX2) and resulting in defective phagocyte-derived reactive oxygen species (ROS) production. Almost 50% of patients with CGD have inflammatory bowel disease (IBD) associated with dysbiosis and age of IBD onset may vary according to CGD genotype. While we previously demonstrated that the intestinal microbiota determines colitis susceptibility in CGD mice, underlying mechanisms remain unknown. We hypothesized that NOX2 defects are associated with distinct intestinal microbiome signatures and immune responses, which impact colitis severity. Chemical colitis susceptibility was evaluated in 2 strains of CGD mice (gp91phox-/- and p47phox-/-) with distinct microbiota, from 2 different animal facilities, while also evaluating the impact of microbiota standardization and colitogenic microbiota transfer on mucosal immune responses at the intestinal barrier. While p47phox-/- and gp91phox-/-mice harbouring colitogenic microbiota had increased colitis severity, the intestinal epithelial cells from p47phox-/- mice produced more ROS which was associated with increased NOX isoform gene expression. In contrast, gp91phox-/- mice had decreased mucin production and a mucosal immune response profile suggestive of increased inflammasome activation at the intestinal barrier compared to control and p47phox-/- mice. Our findings suggest that the microbiota impacts colitis susceptibility in a CGD genotype-specific manner, thereby potentially explaining differences in the timing of IBD onset in patients with different CGD genotypes while identifying potential novel and personalized therapeutic targets.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"24 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143846361","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 individualize treatment for chronic-phase CML.

IF 20.3 1区医学

Blood Pub Date : 2025-04-16 DOI: 10.1182/blood.2024026508

Ariel Monet Leyte-Vidal,Neil P Shah

引用次数: 0

International Consensus Statement on Diagnosis, Evaluation, and Research of Richter Transformation: the ERIC Recommendations.

IF 20.3 1区医学

Blood Pub Date : 2025-04-16 DOI: 10.1182/blood.2024028064

Adam S Kittai,Monia Marchetti,Othman Al-Sawaf,Ohad Benjamini,Alexey V Danilov,Matthew S Davids,Barbara F Eichhorst,Toby A Eyre,Anna Maria Frustaci,Michael J Hallek,Paul Joseph Hampel,Yair Herishanu,Rodney John Hicks,Arnon P Kater,Rebecca L King,José-Ignacio Ignacio Martín-Subero,Carolyn Owen,Erin M Parry,Maurilio Ponzoni,Davide Rossi,Tanya Siddiqi,Stephan Stilgenbauer,Constantine S Tam,Elisa Ten Hacken,Philip A Thompson,William G Wierda,Gianluca Gaidano,Jennifer A Woyach,Paolo Ghia

{"title":"International Consensus Statement on Diagnosis, Evaluation, and Research of Richter Transformation: the ERIC Recommendations.","authors":"Adam S Kittai,Monia Marchetti,Othman Al-Sawaf,Ohad Benjamini,Alexey V Danilov,Matthew S Davids,Barbara F Eichhorst,Toby A Eyre,Anna Maria Frustaci,Michael J Hallek,Paul Joseph Hampel,Yair Herishanu,Rodney John Hicks,Arnon P Kater,Rebecca L King,José-Ignacio Ignacio Martín-Subero,Carolyn Owen,Erin M Parry,Maurilio Ponzoni,Davide Rossi,Tanya Siddiqi,Stephan Stilgenbauer,Constantine S Tam,Elisa Ten Hacken,Philip A Thompson,William G Wierda,Gianluca Gaidano,Jennifer A Woyach,Paolo Ghia","doi":"10.1182/blood.2024028064","DOIUrl":"https://doi.org/10.1182/blood.2024028064","url":null,"abstract":"Richter transformation (RT) is defined as an aggressive lymphoma emerging in patients with chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL). Despite novel therapeutics developed in CLL, RT is associated with poor outcomes. In light of recent progress regarding the diagnostic procedures and therapeutic concepts of RT, an international group of experts, under the coordination of the European Research Initiative on CLL (ERIC), has developed consensus recommendations for clinical procedures and future research on this disease. Patients with RT typically present with a rapid clinical decline, worsening B-symptoms, elevated LDH, and/or rapidly enlarging lymphadenopathy. Workup should include a PET-CT for patients with suspected RT. An excisional biopsy should be taken from an accessible lesion, preferably with the highest FDG avidity, and analyzed for the presence of aggressive lymphoma. The molecular relationship to the original CLL clone(s) should be defined. As no effective standard treatment for RT exists, patients should be treated in a clinical trial. Response of both RT and CLL should be assessed at an early time point, and survival endpoints should be prioritized in trial design. We hope that these recommendations can help to harmonize clinical and translational research and improve outcomes for patients with RT.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"7 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143846363","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

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