Volume 130, Issue 6

Cover Figure: Efficacy and mechanism of action of enasidenib in targeting mutant-IDH2 AML. See the article by Stein et al.

WASHINGTON, August 10, 2017 – 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.

Bifurcated BACH2 control coordinates mantle cell lymphoma survival and dispersal during hypoxia
Zhang and colleagues explore the role of BACH2 in mantle cell lymphoma, demonstrating that BACH2 functions as a tumor repressor and is regulated by hypoxia via the hypoxia-induced factor 1α pathway.

How I use laboratory monitoring of antiplatelet therapy
In a How I Treat article, Michelson and Bhatt review the basics of platelet function and inhibition by antiplatelet agents before focusing on 2 cases that raise the question of testing for aspirin or clopidogrel resistance.

Dysfunctional diversity of p53 proteins in adult acute myeloid leukemia: projections on diagnostic workup and therapy
Somatic p53 mutation is seen in a fraction of AML. In a Perspective, Prokocimer and colleagues discuss the role of other processes leading to p53 disruption in AML, presenting the range of mechanisms by which p53 may be functionally inactivated and the implications for the approach to potential detection and treatment of functional p53 insufficiency.

Enasidenib in mutant IDH2 relapsed or refractory acute myeloid leukemia


Enasidenib induces acute myeloid leukemia cell differentiation to promote clinical response
In companion papers, Stein et al and Amatangelo et al report on a phase 1/2 study targeting mutant IDH2 relapsed/refractory acute myeloid leukemia (AML) with a novel first-in-class inhibitor. Stein et al describe encouraging clinical outcomes with a 40% overall response rate, of which nearly half are complete responses. Amatangelo et al examine enasidenib’s mechanism of action in relation to the biology and the genetic profile of AML and the apparent differentiation-inducing effect that the IDH2 inhibitor exerts on AML blasts.

Clonal hematopoiesis, with and without candidate driver mutations, is common in the elderly


DNMT3A and TET2 dominate clonal hematopoiesis, demonstrate benign phenotypes and different genetic predisposition
In companion papers, Zink et al and Buscarlet et al provide further insight into clonal hematopoiesis of indeterminate potential (CHIP). Together they demonstrate that CHIP, with or without a somatic driver mutation, is much more common than previously reported, may have a familial/genetic predisposition, and likely confers a heterogeneous increased risk of development of hematologic malignancy.


This week's complete table of contents

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