Issue 18, Volume 128

Cover Figure: In vivo transduction of mouse HSPCs following IV injection of adenovirus vectors. See the article by Richter et al.

WASHINGTON, November 3, 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.

Outcomes of CLL patients treated with sequential kinase inhibitor therapy: a real world experience
Mato and colleagues report a retrospective study of clinical outcomes of 178 chronic lymphocytic leukemia (CLL) patients who discontinued kinase inhibitor (KI) therapy with ibrutinib or idelalisib. Toxicity is the leading cause of discontinuation of the therapy, but patients may have subsequent responses to an alternate KI.

In vivo transduction of primitive mobilized hematopoietic stem cells after intravenous injection of integrating adenovirus vectors
Current gene therapy depends on transplantation of ex vivo modified hematopoietic stem/progenitor cells (HSPCs). Richter and colleagues report a novel and successful in vivo strategy for gene therapy in a humanized mouse model using IV injection of adenovirus-based vectors, demonstrating long-term HSPC transduction.

MPL expression on AML blasts predicts peripheral blood neutropenia and thrombocytopenia
The basis for peripheral cytopenias in the setting of acute myeloid leukemia (AML) is still unknown. Rauch and colleagues provide data that opposes the hypothesis that blasts physically displace normal stem cells. They present evidence for suppressed hematopoiesis due to cytokine insufficiency arising from scavenging of thrombopoietin (TPO) by blasts expressing MPL, the TPO receptor.

High selective pressure for Notch1 mutations that induce Myc in T-cell acute lymphoblastic leukemia
Activating mutations in Notch1 are common in T-cell acute lymphoblastic leukemia, but Notch inhibitors rarely give sustained control of the disease. Chiang and colleagues examine the mechanism of resistance to Notch inhibition and report that tumors may escape through increased expression of Myc, which is a downstream Notch target and can substitute for Notch.

Evaluation of the potential therapeutic benefits of macrophage reprogramming in multiple myeloma
Tumor-associated macrophages are postulated to provide a supportive environment for multiple myeloma cells in the bone marrow. Gutiérrez-González and colleagues report that manipulation of the cytokine milieu can reprogram macrophages from the M2 to the M1 phenotype, resulting in loss of the immunosuppressive properties that support myeloma-cell survival and proliferation.


This week's complete table of contents

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