Volume 132, Issue 6



August 9, 2018 – 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.

Cover Figure: Structural topology of the interaction between vitamin K epoxide reductase and warfarin. See the article by Wu et al.

Aged murine hematopoietic stem cells drive aging-associated immune remodeling
Leins et al investigate how much the decline of immune function associated with aging is cell intrinsic and how much reflects declining thymic function. In a series of studies in transgenic mice, they demonstrate that functional aging mostly reflects hematopoietic stem cell aging and is independent of thymic function.

Identification of novel mutational drivers reveals oncogene dependencies in multiple myeloma
Walker et al report an integrated genomic analysis of over 1000 patients with newly diagnosed multiple myeloma. They identify a large number of driver genes and demonstrate that driver genes are associated with nonrandom acquisition of specific secondary mutations.

GPIbα is required for platelet-mediated hepatic thrombopoietin generation
Prevailing dogma posits that thrombopoietin (TPO) production is constitutive and is regulated by binding and clearance by platelets and megakaryocytes. Xu et al present compelling data for a novel mechanism for TPO regulation, demonstrating that platelet GPIbα induces hepatic TPO transcription, thereby explaining why patients with Bernard-Soulier syndrome have low TPO levels.

Hematopoiesis and the bacterial microbiome
In a Blood Spotlight, Yan and colleagues provide a timely update on the role of the products from gut flora that signal to the bone marrow. The authors also discuss the important role that dysbiosis plays in cytopenias associated with inflammatory bowel disease, obesity, and antibiotic treatment.

Syndromic congenital myelofibrosis associated with a loss-of-function variant in RBSN
Magoulas and colleagues describe a complex clinical syndrome associated with mutations in RBSN, characterized by severe neutropenia, neurocognitive disorders, and congenital myelofibrosis.

Srsf2P95H initiates myeloid bias and myelodysplastic/myeloproliferative syndrome from hemopoietic stem cells
SRSF2M mutations are found in myelodysplastic syndromes (MDS) and in MDS/myeloproliferative neoplasm (MPN) overlap syndromes and are also identified in age-related clonal hematopoiesis. Using an inducible model of mutant Srsf2P95H, Smeets et al demonstrate that the mutant gene, when expressed in stem cells, is sufficient to induce myeloid skewing, and with aging, progression to MDS/MPN overlap syndromes.

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