Volume 134, Issue 10



September 5, 2019 – Welcome to “This Week in Blood,” a weekly snapshot of the hottest studies from each week’s issue of Blood, the official journal of the American Society of Hematology (ASH), hand-picked by Blood Editor-in-Chief Bob Löwenberg, MD, PhD, and Deputy Editor Nancy Berliner, MD.

Cover Figure:Increased SLAMF7high monocytes in myelofibrosis patients harboring JAK2V617F provide a therapeutic target of elotuzumab. See the article by Maekawa et al.

Early progression as a predictor of survival in marginal zone lymphomas: an analysis from the FIL-NF10 study
Luminari and colleagues demonstrate that in patients with marginal zone lymphoma requiring therapy at presentation, progression within 24 months predicts for markedly inferior survival.

Shared roles for Scl and Lyl1 in murine platelet production and function
Stem cell leukemia (Scl) protein is part of a 4-protein transcription factor complex required for megakaryopoiesis, but mutated Scl does not cause thrombocytopenia. Chiu and colleagues used conditional knockout mice to demonstrate that lymphoblastic leukemia 1 (Lyl1) can substitute for Scl and that this functional redundancy explains why mutations in either gene alone do not decrease platelet production.

Integrative genomic analysis identifies key pathogenic mechanisms in primary mediastinal large B-cell lymphoma
Mottok et al present the genomic landscape of primary mediastinal large B-cell lymphoma (PMBL), identifying key driver genes and providing evidence that PMBL is distinct from diffuse large B-cell lymphoma and more closely related to classical Hodgkin lymphoma..

Genetic defects in hematopoietic transcription factors and predisposition to acute lymphoblastic leukemia
In this Blood Spotlight, Gocho and Yang highlight new insights into the genetic basis for acute lymphoblastic leukemia.

Increased SLAMF7high monocytes in myelofibrosis patients harboring JAK2V617F provide a therapeutic target of elotuzumab
In myelofibrosis (MF), JAK2V617F-positive monocytes differentiate into fibrocytes that contribute to marrow fibrosis. Maekawa et al demonstrate that these monocytes express increased SLAMF7 and are increased in the peripheral blood of patients with MF; furthermore, SLAMF7 inhibition reduces fibrosis in a mouse model of MF.

View this week's complete table of contents

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