Issue Archive
Table of Contents
INSIDE BLOOD
PLENARY PAPERS
C-terminal ADAMTS-18 fragment induces oxidative platelet fragmentation, dissolves platelet aggregates, and protects against carotid artery occlusion and cerebral stroke
REVIEW ARTICLES
CLINICAL TRIALS AND OBSERVATIONS
Differential efficacy of bortezomib plus chemotherapy within molecular subtypes of diffuse large B-cell lymphoma
Clinical Trials & Observations
Methotrexate/6-mercaptopurine maintenance therapy influences the risk of a second malignant neoplasm after childhood acute lymphoblastic leukemia: results from the NOPHO ALL-92 study
Clinical Trials & Observations
HEMATOPOIESIS AND STEM CELLS
IMMUNOBIOLOGY
Plasmacytoid dendritic cells accumulate in spleens from chronically HIV-infected patients but barely participate in interferon-α expression
LYMPHOID NEOPLASIA
MYELOID NEOPLASIA
Frequent CBL mutations associated with 11q acquired uniparental disomy in myeloproliferative neoplasms
Targeting the leukemia microenvironment by CXCR4 inhibition overcomes resistance to kinase inhibitors and chemotherapy in AML
RED CELLS, IRON, AND ERYTHROPOIESIS
Hepcidin, the hormone of iron metabolism, is bound specifically to α-2-macroglobulin in blood
VASCULAR BIOLOGY
CORRESPONDENCE
Response: Could mutations in the hypoxanthine-guanine phosphoribosyl transferase gene induced by thiopurine therapy promote the development of second malignant neoplasms?
RETRACTIONS
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Cover Image
Cover Image
Tiam1 is a Rac activator involved in PKCζ/Par polarity signaling, essential for stabilization of polarization during T-cell migration. T cells (green) crawl on top of endothelial monolayers (purple) to reach suitable transmigration sites at endothelial junctions (paracellular migration). Tiam1-deficient T cells are unable to crawl on endothelial cells and, as a consequence, initiate an alternative transmigration route through individual endothelial cells (transcellular migration). This suggests that T cells are able to change their route of transendothelial migration according to their polarization status and crawling capacity. See the article by Gérard et al on page 6138.
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Response: Could mutations in the hypoxanthine-guanine phosphoribosyl transferase gene induced by thiopurine therapy promote the development of second malignant neoplasms?