Thrombosis in myeloproliferative neoplasms with JAK2V617F mutation

Clin Appl Thromb Hemost. 2013 Jul-Aug;19(4):374-81. doi: 10.1177/1076029612453761. Epub 2012 Jul 23.

Abstract

Myeloproliferative neoplasms (MPNs) are clonal hematopoietic stem cell disorders and are characterized by advanced proliferation and survival advantage. These abnormalities are considered to derive from the point mutation in exon 14 of the Janus kinase 2 genes (JAK2 V617F). The thrombosis rate and the high prevalence of JAK2V617F in patients with MPN suggest that there is an association between the 2 in MPN. Apart from the mutation, other variables are documented to cause endothelial dysfunction and involve in thrombotic tendency. Endothelial progenitor cells differentiated from hematopoietic stem cell in patients with JAK2V617F MPN play an indispensable role in initiating and modulating neoangiogenesis. Although a risk-oriented therapeutic approach has been applied to MPN treatments, the further study on pathogenesis of MPN may provide more novel preventions and therapies for MPN.

Keywords: JAK2V617F mutation; endothelial progenitor cells; myeloproliferative neoplasms; thrombosis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Humans
  • Janus Kinase 2 / blood
  • Janus Kinase 2 / genetics*
  • Myeloproliferative Disorders / enzymology*
  • Myeloproliferative Disorders / genetics*
  • Myeloproliferative Disorders / pathology
  • Point Mutation*
  • Risk Factors
  • Thrombosis / enzymology*
  • Thrombosis / genetics*
  • Thrombosis / pathology

Substances

  • JAK2 protein, human
  • Janus Kinase 2