Advertisement

Volume 133, Issue 22

 

 

May 30, 2019 – 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: Trib1 regulates eosinophil lineage development. See the article by Mack et al.

Cleavage of anti-PF4/heparin IgG by a bacterial protease and potential benefit in heparin-induced Thrombocytopenia
Heparin-induced thrombocytopenia (HIT) is caused by immunoglobulin G (IgG) antibodies that bind platelet factor 4 and activate platelets via FcgRIIa receptors. Kizlik-Masson et al demonstrate that IdeS, a bacterial protease from Streptococcus pyogenes that cleaves the heavy chain of IgG and abolishes FcgR binding, cleaves HIT antibodies and abolishes heparin-dependent platelet activation, offering a potential new therapy for severe HIT.


Hydroxyurea reduces cerebral metabolic stress in patients with sickle cell anemia
Fields and colleagues examined the oxygen extraction fraction (OEF) as a marker of cerebral metabolic stress in patients with sickle cell anemia who were receiving no disease-modifying therapy, hydroxyurea therapy, or chronic transfusion therapy. They demonstrate that while cerebral blood flow was the same for all three groups, the OEF was highest in patients on no therapy, lower in patients on hydroxyurea, and lowest in patients on transfusion therapy.


Dysfunctional endogenous FIX impairs prophylaxis in a mouse hemophilia B model
Most patients with hemophilia B have mutations in the factor IX (FIX) gene which lead to a protein that is functionally inactive. Using mouse models of hemophilia B, Cooley et al demonstrate that this circulating species impairs response to FIX prophylaxis, perhaps explaining the wide range of individual responses to infused FIX products in patients with hemophilia B.


Trib1 regulates eosinophil lineage commitment and identity by restraining the neutrophil program
Mack and colleagues demonstrate that Trib1 is critical for eosinophil development, promoting eosinophil lineage commitment and suppressing neutrophil differentiation.


Tumor-educated platelets
In ‘t Veld and Wurdinger review the use of tumor-educated platelets as a source of biomarkers for “liquid biopsies” for the diagnosis and follow-up of cancer.


How I treat chronic myeloid leukemia in children and adolescents
Hijiya and Suttorp use 4 illustrative cases to describe the unique issues in the treatment of chronic myeloid leukemia in children and adolescents.


RNA-binding proteins in hematopoiesis and hematological malignancy
Hodson et al review the essential role of RNA-binding proteins in regulating RNA abundance and modification. The authors describe the essential role of these proteins in normal hematopoiesis, as well as their potential functions as oncoproteins and tumor suppressors.

View this week's complete table of contents

Why Submit to Blood?

 


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.