Issue Archive
Table of Contents
INSIDE BLOOD COMMENTARIES
PLENARY PAPER
Acute myeloid leukemia ontogeny is defined by distinct somatic mutations
PERSPECTIVES
BLOOD SPOTLIGHT
HOW I TREAT
CLINICAL TRIALS AND OBSERVATIONS
Brentuximab vedotin demonstrates objective responses in a phase 2 study of relapsed/refractory DLBCL with variable CD30 expression
Clinical Trials & Observations
R-MPV followed by high-dose chemotherapy with TBC and autologous stem-cell transplant for newly diagnosed primary CNS lymphoma
Clinical Trials & Observations
Pomalidomide plus low-dose dexamethasone in multiple myeloma with deletion 17p and/or translocation (4;14): IFM 2010-02 trial results
Clinical Trials & Observations
HEMATOPOIESIS AND STEM CELLS
Notch1 acts via Foxc2 to promote definitive hematopoiesis via effects on hemogenic endothelium
IMMUNOBIOLOGY
LYMPHOID NEOPLASIA
PHAGOCYTES, GRANULOCYTES, AND MYELOPOIESIS
PLATELETS AND THROMBOPOIESIS
RED CELLS, IRON, AND ERYTHROPOIESIS
THROMBOSIS AND HEMOSTASIS
TRANSPLANTATION
Ex vivo fucosylation of third-party human regulatory T cells enhances anti–graft-versus-host disease potency in vivo
Brief Report
BLOOD WORK
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Cover Image
Cover Image
Smooth muscle cells produce a pathological hyaluronan matrix (green) typified by cable-like structures when activated with the viral mimetic polyI:C or a number of other agents. Platelets (immunohistochemically stained red for CD42b) have the ability to bind to hyaluronan cables. Additionally, they carry the hyaluronan-degrading enzyme HYAL2 in their α granules. Upon activation, platelets rapidly transpose the enzyme to their surface, thus putting enzyme and substrate in close proximity. This results in hyaluronan matrix degradation. In this experiment, hyaluronan removal is blocked with any antibody to HYAL2. See the article by Albeiroti et al on page 1460.
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