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Issue 17, Volume 127

Cover Figure: Normal ABL1 as a tumor suppressor and therapeutic target. See the article by Dasgupta et al.

WASHINGTON, April 28,  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.

Dexamethasone vs prednisone in induction treatment of pediatric ALL: results of the randomized trial AIEOP-BFM ALL 2000
Möricke and colleagues report clinically important findings from a large cooperative clinical trial in acute lymphoblastic leukemia. They demonstrate that substituting dexamethasone for prednisone during induction chemotherapy in children and adolescents improves event-free survival, although it has no impact on overall survival.

Clinical impact of clonal and subclonal TP53, SF3B1, BIRC3, NOTCH1 and ATM mutations in chronic lymphocytic leukemia
Nadeu and colleagues delve deep into the genomes of patients diagnosed with chronic lymphocytic leukemia. Their ultradeep sequencing data reveal remarkably heterogeneous clonal and subclonal mutations and demonstrate that, for particular genes, the size of the mutant clone has profound clinical implications.

Introduction to a review series: the paradox of indolent B-cell lymphoma
The articles within a comprehensive series of 5 reviews by leaders in the field explore the unique biology and management aspects of indolent B-cell lymphoma subtypes.
The articles in this review series, "The paradox of indolent B-cell lymphoma," include the following:

Polygenic mutations in the cytotoxicity pathway increase susceptibility to develop HLH immunopathology in mice
The pathogenesis in some patients with hemophagocytic lymphohistiocytosis (HLH) is related to autosomal recessive mutations in genes required for lymphocyte cytotoxicity. The study by Sepulveda and colleagues shows that heterozygous mutations in different HLH-associated genes are additive and confer increased risk of developing disease.

Normal ABL1 is a tumor suppressor and therapeutic target in human and mouse leukemias expressing oncogenic ABL1 kinases
Dasgupta et al provide genetic evidence for an inhibitory role of normal ABL1 in BCR-ABL–induced chronic myeloid leukemia. Their data imply that normal ABL1 kinase behaves like a tumor suppressor. Enhancing the activity of normal ABL1 may be therapeutic in leukemias expressing oncogenic forms of the kinase.

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.

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