Issue Archive
Table of Contents
Inside Blood
Plenary Paper
Hypoxia-inducible factors in human pulmonary arterial hypertension: a link to the intrinsic myeloid abnormalities
How I Treat
Clinical Trials and Observations
The clinical utility and prognostic value of multiparameter flow cytometry immunophenotyping in light-chain amyloidosis
Brief Report
Hematopoiesis and Stem Cells
Immunobiology
Lymphoid Neoplasia
Chemotherapeutic agents circumvent emergence of dasatinib-resistant BCR-ABL kinase mutations in a precise mouse model of Philadelphia chromosome–positive acute lymphoblastic leukemia
Gene expression analysis uncovers similarity and differences among Burkitt lymphoma subtypes
Myeloid Neoplasia
Phagocytes, Granulocytes, and Myelopoiesis
Platelets and Thrombopoiesis
Red Cells, Iron, and Erythropoiesis
Global gene expression analysis of human erythroid progenitors
e-blood
Thrombosis and Hemostasis
KNG1 Ile581Thr and susceptibility to venous thrombosis
Brief Report
Transplantation
Results of allogeneic hematopoietic stem cell transplantation for chronic myelogenous leukemia patients who failed tyrosine kinase inhibitors after developing BCR-ABL1 kinase domain mutations
Clinical Trials & Observations
Correspondence
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Cover Image
Cover Image
The cover image shows the interdependence of pulmonary angioproliferative remodeling and a bone marrow myeloproliferative process in pulmonary arterial hypertension. Hypoxia-induced factors that are released by the lung endothelium promote proliferation and mobilization of bone marrow progenitors and myelofibrosis. Likewise, myeloid progenitors recruited into the lung fuel the proliferative angiopathy. The cover image is a montage of the myelopulmonary model superimposed on histopathology of bone marrow tissue section stained for reticulin (in black) from a patient with primary pulmonary hypertension. See the article by Farha et al on page 3485.
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