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Issue 21, Volume 127

Cover Figure: Challenging the current notions about the players in spontaneous thrombosis. See the article by Heestermans et al.

WASHINGTON, May 26,  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.

Targeted gene editing restores regulated CD40L function in X-linked hyper-IgM syndrome
In their plenary paper in this week’s Blood, Hubbard et al provide an innovative approach of genome editing to knock in a wild-type cDNA and functionally correct disease-causing mutations in a gene in primary human T cells. The level of gene editing appears high enough to potentially allow therapeutic correction of primary immunodeficiency.

VTD is superior to VCD prior to intensive therapy in multiple myeloma: results of the prospective IFM2013-04 trial
In an important clinical trial, Moreau et al compared bortezomib-thalidomide-dexamethasone (VTD) to bortezomib-cyclophosphamide-dexamethasone (VCD) as induction before high-dose therapy and autologous stem cell transplantation in patients with newly diagnosed multiple myeloma. The ramifications are broad. Their data show that the VTD regimen is markedly superior for newly diagnosed myeloma.

Exome sequencing reveals recurrent germ line variants in patients with familial Waldenström macroglobulinemia
In this issue of Blood, Roccaro et al report the possible contribution of the germ line genetic variants LAPTM5c403t and HCLS1g496a to inherited susceptibility to familial Waldenström macroglobulinemia.

Welcoming a new age for gene therapy in hematology
The exciting new field of genome editing represents a quantum leap for biology and medicine. A series of four reviews written by experts in the field summarize conceptual, clinical, and ethical aspects of genome editing with a focus on its potential for treating hematologic diseases.
The articles in this review series, "Genome Editing in Hematology, " include the following:

Role of platelets, neutrophils, and factor XII in spontaneous venous thrombosis in mice
Heestermans et al examined the roles of platelets, neutrophils and FXII in a new genetic mouse model of spontaneous venous thrombosis. Their data profoundly challenge the current notions about these players in venous thrombosis.

Novel phosphatidylethanolamine derivatives accumulate in circulation in hyperlipidemic ApoE−/− mice and activate platelets via TLR2
Biswas and colleagues show that a group of oxidized lipid species are a new type of platelet agonists that induce platelet activation via a TLR2 receptor pathway. They induce cross talk between innate immunity and integrin activation signaling pathways. These data are directly relevant to the atherothrombosis field.

 

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.