JAK2V617F-mutant vascular niche contributes to JAK2V617F clonal expansion in myeloproliferative neoplasms
نویسندگان
چکیده
منابع مشابه
TNFα facilitates clonal expansion of JAK2V617F positive cells in myeloproliferative neoplasms.
Proinflammatory cytokines such as TNFα are elevated in patients with myeloproliferative neoplasms (MPN), but their contribution to disease pathogenesis is unknown. Here we reveal a central role for TNFα in promoting clonal dominance of JAK2(V617F) expressing cells in MPN. We show that JAK2(V617F) kinase regulates TNFα expression in cell lines and primary MPN cells and TNFα expression is correla...
متن کاملMYELOID NEOPLASIA TNF facilitates clonal expansion of JAK2V617F positive cells in myeloproliferative neoplasms
1Division of Hematology and Medical Oncology, Oregon Health & Science University (OHSU) Knight Cancer Institute, Portland, OR; 2Department of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Vienna, Austria; 3Division of Pediatric Hematology and Oncology, Department of Pediatrics, OHSU, Portland, OR; 4Department of Pathology, OSHU, Portland, OR; 5Cen...
متن کاملPrognostic significance of ASXL1, JAK2V617F mutations and JAK2V617F allele burden in Philadelphia-negative myeloproliferative neoplasms
BACKGROUND Despite insights into the genetic basis of Philadelphia-negative myeloproliferative neoplasms (Ph-negative MPNs), a significant proportion of essential thrombocythemia (ET) and primary myelofibrosis (PMF) patients present with no known MPN disease alleles. There were no previous studies investigating the impact of ASXL1 mutations in Ph-negative MPNs in Turkey. In the current study, w...
متن کاملHow does JAK2V617F contribute to the pathogenesis of myeloproliferative neoplasms?
A decade on from the discovery of the JAK2V617F mutation in the majority of patients with myeloproliferative neoplasms (MPNs), JAK2V617F is now firmly installed in the hematology curriculum of medical students and the diagnostic-testing algorithm of clinicians. Furthermore, the oral JAK1/JAK2 inhibitor ruxolitinib, rationally designed to target activated JAK2 signaling in MPN, has been approved...
متن کاملJAK2V617F-homozygosity drives a phenotypic switch between myeloproliferative neoplasms in a murine model, but is insufficient to sustain clonal expansion
Genomic regions of acquired uniparental disomy (UPD) are common in malignancy and frequently harbor mutated oncogenes. Homozygosity for such gain-of-function mutations is thought to modulate tumor phenotype, but direct evidence has been elusive. Polycythemia vera (PV) and essential thrombocythemia (ET), two subtypes of myeloproliferative neoplasms, are associated with an identical acquired JAK2...
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ژورنال
عنوان ژورنال: Blood Cells, Molecules, and Diseases
سال: 2016
ISSN: 1079-9796
DOI: 10.1016/j.bcmd.2016.09.004