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Issue 22, Volume 127

Cover Figure: B-cell conditional expression of mutant Myd88 models DLBCL in mice. See the article by Knittel et al.

WASHINGTON, June 2,  2016 – 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.

Revised classification of histiocytoses and neoplasms of the macrophage-dendritic cell lineages
The histiocytoses are a collection of over 100 rare and heterogeneous disorders associated with the accumulation of macrophages, dendritic cells, and monocytes. Emile and colleagues integrate new findings related to clinical, genetic, and histologic features of these disorders to propose a revised classification system dividing histiocytoses into 5 groups of diseases.

Disturbed sialic acid recognition on endothelial cells and platelets in complement attack causes atypical hemolytic uremic syndrome
Atypical hemolytic uremic syndrome (aHUS) is associated with uncontrolled complement activation. It is often associated with mutations in factor H, a complement-inhibitory protein. Hyvärinen and colleagues demonstrate that complement inhibition by factor H requires binding of the protein to both C3b and sialic acid, and mutations in patients with aHUS usually impair sialic acid binding. Since many bacteria secrete sialidases, these studies provide critical insights into the interaction of infection with predisposing factor H mutations in triggering aHUS.

Risk stratification of chromosomal abnormalities in chronic myelogenous leukemia in the era of tyrosine kinase inhibitor therapy
Wang and colleagues reassess the prognostic importance of additional chromosomal abnormalities (ACAs) in patients with chronic-phase chronic myelogenous leukemia. Their study reveals how complex the landscape is: there are differences in impact for “good” and “poor” prognostic changes, but also divergent prognoses for ACAs that are present at diagnosis versus those acquired during treatment with tyrosine kinase inhibitors.

Fibrin deposition following bile duct injury limits fibrosis through an αMβ2-dependent mechanism
Activation of coagulation and fibrin deposition has been implicated in many forms of liver disease. Joshi and colleagues examine the effect of disrupting fibrinogen interaction with leukocyte αMβ2receptors in a mouse model of chemical-induced hepatic injury. They make the paradoxical observation that disrupting this interaction actually increases fibrosis, and they conclude that this interaction inhibits bile duct injury–related fibrosis. This offers a potential new pathway for intervening in cholestatic liver disease.

Personalized medicine in thrombosis: back to the future
In their Perspective article, Nagalla and Bray discuss the concept of personalized medicine in the context of thrombotic disease. While supporting the importance of genomic approaches to understanding thrombosis, they contend that genomic observations have not yet had a significant impact on the practice of medicine in this realm. They suggest that current approaches be “personalized” through a careful history and physical and judicious laboratory testing.

This week's complete table of contents

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Blood (www.bloodjournal.org), the most cited peer-reviewed publication in the field of hematology, is available weekly in print and online. Blood is the official journal of the American Society of Hematology (ASH) (www.hematology.org), the world’s largest professional society concerned with the causes and treatment of blood disorders.

ASH’s mission is to further the understanding, diagnosis, treatment, and prevention of disorders affecting blood, bone marrow, and the immunologic, hemostatic, and vascular systems by promoting research, clinical care, education, training, and advocacy in hematology.

blood® is a registered trademark of the American Society of Hematology.