Issue Archive
Table of Contents
INSIDE BLOOD COMMENTARIES
PLENARY PAPER
Early-onset lymphoproliferation and autoimmunity caused by germline STAT3 gain-of-function mutations
PERSPECTIVES
The hidden genomic landscape of acute myeloid leukemia: subclonal structure revealed by undetected mutations
HOW I TREAT
CLINICAL TRIALS AND OBSERVATIONS
Drug-induced thrombotic microangiopathy: a systematic review of published reports
Clinical Trials & Observations
Brief Report
HEMATOPOIESIS AND STEM CELLS
IMMUNOBIOLOGY
Autoimmunity, hypogammaglobulinemia, lymphoproliferation, and mycobacterial disease in patients with activating mutations in STAT3
Clinical Trials & Observations
LYMPHOID NEOPLASIA
BCL2 mutations are associated with increased risk of transformation and shortened survival in follicular lymphoma
Clinical Trials & Observations
A genome-wide association study of susceptibility to acute lymphoblastic leukemia in adolescents and young adults
Clinical Trials & Observations
PHAGOCYTES, GRANULOCYTES, AND MYELOPOIESIS
PLATELETS AND THROMBOPOIESIS
RED CELLS, IRON, AND ERYTHROPOIESIS
THROMBOSIS AND HEMOSTASIS
TRANSPLANTATION
CMV promotes recipient T-cell immunity following reduced-intensity T-cell–depleted HSCT, significantly modulating chimerism status
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Cover Image
Cover Image
Does the contact activation defect in prekallikrein deficiency protect from collagen/epinephrine (Col/Epi)-induced pulmonary emboli? This immunofluorescence image is of pulmonary microthrombi from prekallikrein-null (Klkb1−/−) mice following treatment with intravenous Col/Epi. The green color stains fibrin (Mab 59D8), the red color stains platelets (Mab anti-CD42c), and the orange color reflects their colocalization. Klkb1−/− mice have microvessel fibrin-platelet pulmonary emboli identical to those of wild-type mice (not shown), indicating that the mechanism for thrombosis observed is not mediated through contact activation. See the article by Stavrou et al on page 710.
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