JAK2V617F mutation in immune thrombocytopenia.

Thromb Res

Division of Hematology and Oncology, Department of Medicine, Chang Gung Memorial Hospital, Chiayi, Taiwan; College of Medicine, Chang Gung University, Tao-Yuan, Taiwan. Electronic address:

Published: August 2016


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.thromres.2016.06.019DOI Listing

Publication Analysis

Top Keywords

jak2v617f mutation
4
mutation immune
4
immune thrombocytopenia
4
jak2v617f
1
immune
1
thrombocytopenia
1

Similar Publications

The prevalence of paroxysmal nocturnal hemoglobinuria (PNH) clones is little investigated in myeloproliferative neoplasms (MPN) patients. The aim of this multicenter study was to evaluate the prevalence of PNH clones (glycosyl-phosphatidyl-inositol lacking) in 119 Ph- negative MPN patients having anemia, LDH elevation, asthenia and history of thrombosis. All the participating centers performed the standardized diagnostic test by using a single lyophilized template for granulocytes, monocytes, and erythrocytes.

View Article and Find Full Text PDF

The acquired JAK2-V617F mutation plays a causal role in myeloproliferative neoplasms (MPN). Weakly activating JAK2 germline variants have been associated with MPN risk, but the underlying mechanisms remain unclear. We previously identified the JAK2-R1063H germline variant, which contributes to hereditary MPN and increased disease severity in essential thrombocythemia.

View Article and Find Full Text PDF

Platelet Jak2-deficiency accelerates atherosclerosis with increased inflammatory response.

J Biol Chem

August 2025

Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, M5G 2C4, Canada; Department of Immunology, University of Toronto, Toronto, Ontario, M5G 2M9, Canada; Institute of Medical Science and Department of Pharmacology and Toxicology, University of Toronto, Toronto, O

Cardiovascular disease (CVD) is the leading cause of mortality worldwide, of which atherosclerosis is the major pathology. Chronic inflammation underlies atherosclerosis, and Janus kinase 2 (Jak2) is a critical signaling node that mediates this process. Jak2 activating mutation has recently been implicated in clonal hematopoiesis of indeterminate potential as an emerging major CVD risk factor.

View Article and Find Full Text PDF

Background: Clonal evolution drives progression of myeloproliferative neoplasms (MPN) from chronic phase (CP) to blastic phase (BP).

Methods: Targeted next-generation sequencing of 46 paired MPN-CP/BP samples was performed to assess clonal evolution through variant allele frequency changes.

Results: The median time from MPN-CP to BP was 6.

View Article and Find Full Text PDF

Background: The JAK2-V617F mutation is the most frequent driver mutation in a group of malignant hematopoietic disorders called myeloproliferative neoplasms (MPN). JAK2-V617F is a somatic mutation originating in a hematopoietic stem cell and results in constitutively activated JAK-STAT signaling. High levels of pro-inflammatory cytokines in the blood are a hallmark of MPN patients and are a key factor in the severe clinical symptoms seen in these patients.

View Article and Find Full Text PDF