
Activation of JAK/STAT Signaling in Megakaryocytes Sustains Myeloproliferation In Vivo
Author(s) -
Brittany A. Woods,
Wei Chen,
Sophia Chiu,
Christian Marinaccio,
Chunling Fu,
Lilly Gu,
Marinka Bulic,
Qiong Yang,
Anouar Zouak,
Shengxian Jia,
Praveen Suraneni,
Kailin Xu,
Ross L. Levine,
John D. Crispino,
Qiang Wen
Publication year - 2019
Publication title -
clinical cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.427
H-Index - 324
eISSN - 1557-3265
pISSN - 1078-0432
DOI - 10.1158/1078-0432.ccr-18-4089
Subject(s) - megakaryocyte , erythropoiesis , thrombocytosis , haematopoiesis , myelofibrosis , polycythemia vera , essential thrombocythemia , biology , cancer research , thrombopoietin , bone marrow , thrombopoietin receptor , megakaryocytopoiesis , ruxolitinib , janus kinase 2 , myeloproliferative disorders , immunology , myeloid , leukocytosis , myelopoiesis , stem cell , signal transduction , medicine , microbiology and biotechnology , platelet , anemia
The myeloproliferative neoplasms (MPN), including polycythemia vera, essential thrombocythemia, and primary myelofibrosis, are characterized by the expansion of the erythroid, megakaryocytic, and granulocytic lineages. A common feature of these disorders is the presence of abnormal megakaryocytes, which have been implicated as causative agents in the development of bone marrow fibrosis. However, the specific contributions of megakaryocytes to MPN pathogenesis remain unclear.
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