Issue Archive
Table of Contents
Inside Blood
Blood Work
Plenary Paper
Perspectives
Biologic and clinical significance of somatic mutations of SF3B1 in myeloid and lymphoid neoplasms
Review Article
Clinical Trials and Observations
Outcome and pathologic classification of children and adolescents with mediastinal large B-cell lymphoma treated with FAB/LMB96 mature B-NHL therapy
Clinical Trials & Observations
Immunobiology
Lymphoid Neoplasia
Clinical drug resistance linked to interconvertible phenotypic and functional states of tumor-propagating cells in multiple myeloma
Allogeneic, but not autologous, hematopoietic cell transplantation improves survival only among younger adults with acute lymphoblastic leukemia in first remission: an individual patient data meta-analysis
Clinical Trials & Observations
Heat shock protein 70 regulates Tcl1 expression in leukemia and lymphomas
Myeloid Neoplasia
Spleen endothelial cells from patients with myelofibrosis harbor the JAK2V617F mutation
inv(16)/t(16;16) acute myeloid leukemia with non–type A CBFB-MYH11 fusions associate with distinct clinical and genetic features and lack KIT mutations
Vascular Biology
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Cover Image
Cover Image
Hypothetical model for endothelial endoglin in leukocyte transmigration through the vessel endothelium. Upon inflammatory stimulation, soluble factors are released, including the chemokine CXCL12, leading to activation and endoglin-dependent extravasation of leukocytes (A). Leukocyte transmigration involves the binding of CXCL12 to its receptor CXCR4, which in turn activates the β1 integrins. Once activated, β1 integrin binds to the RGD motif of endoglin present on the endothelial cell (EC) surface, allowing the extravasation and migration of leukocytes to the inflammatory site (B). Soluble endoglin competes for the binding between leukocyte β1 integrin and endothelial membrane anchored endoglin, thus interfering with leukocyte adhesion and transmigration (C). See the article by Rossi et al on page 403.
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