| Literature DB >> 30767234 |
Kenneth Kaushansky1, Huichun Zhan1.
Abstract
The hematopoietic niche is composed of endothelial cells, mesenchymal stromal cells of several types, and megakaryocytes, and functions to support the survival, proliferation, and differentiation of normal hematopoietic stem cells (HSCs). An abundance of evidence from a range of hematological malignancies supports the concept that the niche also participates in the pathogenesis of malignant hematopoiesis, differentially supporting malignant stem or progenitor cells over that of normal blood cell development. In 2005, patients with myeloproliferative neoplasms were reported to harbor an acquired, activating, missense V617F mutation of the cytokine-signaling Janus kinase (JAK)-2, JAK2V617F , present in virtually all patients with polycythemia vera and half of patients with essential thrombocythemia and primary myelofibrosis. Using both in vitro and in vivo methods, several investigators have shown that in addition to driving cytokine-independent proliferation in HSCs, JAK2V617F contributes to these neoplasms by altering the hematopoietic niche. The role of both endothelial cells and megakaryocytes bearing JAK2V617F will be presented, which involves altering cytokine production within the niche, resulting in their differential support of mutant kinase-bearing stem cells over their normal counterparts, and imparting relative radiation resistance to stem cells. The clinical correlates of these findings will be discussed, as will their therapeutic implications.Entities:
Keywords: Jak2V617F; endothelial cells; hematopoiesis; hematopoietic niche; hematopoietic stem cells; megakaryocytes; myeloproliferative neoplasms
Year: 2019 PMID: 30767234 PMCID: PMC6814507 DOI: 10.1111/nyas.14028
Source DB: PubMed Journal: Ann N Y Acad Sci ISSN: 0077-8923 Impact factor: 5.691