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Issue 14, Volume 128

Cover Figure: Pivotal role of MCL1 in myeloma cell survival. See the article by Gong et al.

WASHINGTON, October 6, 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.

The antigenic complex in HIT binds to B-cells via complement and complement receptor 2 (CD21)
In this week’s plenary paper, Khandelwal and colleagues demonstrate that the initiating event in patients who develop heparin-induced thrombocytopenia (HIT) is the activation of complement by heparin-PF4 complexes and binding of the complexes to B cells via complement receptor 2 (CR2). These studies may help explain many aspects of the immune response leading to HIT.

Disseminated intravascular coagulation at diagnosis is a strong predictor for thrombosis in acute myeloid leukemia
Libourel and colleagues report that approximately 10% of patients with acute myeloid leukemia develop thrombosis between diagnosis and first consolidation. Elevation of D-dimer greatly increases the risk for thrombosis, suggesting that simple screening could identify patients at high risk for this surprisingly common complication.

Postthrombotic syndrome and other outcomes of lower extremity deep vein thrombosis in children
Avila and colleagues present follow-up on 339 children with lower extremity deep vein thrombosis (DVT) regarding postthrombotic syndrome (PTS), DVT resolution, and other adverse events. Line-related DVT has a better prognosis than non-line-related DVT, and sex, triggering event, and resolution predict for PTS.

Prothrombotic skeletal muscle myosin directly enhances prothrombin activation by binding factors Xa and Va
Deguchi and colleagues demonstrate that myosin enhances thrombosis through direct binding of factors Xa and Va. Furthermore, myosin antibodies inhibit thrombin generation in plasma from acute trauma patients, suggesting a possible etiology for increased thrombosis in acute trauma patients.

Altered fibrinolysis in autosomal dominant thrombomodulin-associated coagulopathy
Burley and colleagues analyze a rare thrombomodulin gene mutation that underlies a recently described rare bleeding disorder. Because it causes increased thrombomodulin levels, bleeding was thought to reflect excessive protein C activation. They report a more complex pathophysiology reflecting both increased protein C activation and inhibition of fibrinolysis through activation of thrombin-activatable fibrinolysis inhibitor (TAFI).

How I diagnose and manage individuals at risk for inherited myeloid malignancies
This “How I Treat” article presents a comprehensive overview of genetic syndromes associated with familial predisposition to myeloid malignancy. The authors discuss key clinical and laboratory issues, addressing how to recognize and care for patients with hereditary myeloid malignancy, and offer recommendations to clinicians in the 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.

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