Focus on the epigenome in the myeloproliferative neoplasms. Review uri icon

Overview

MeSH Major

  • Epigenesis, Genetic
  • Hematologic Neoplasms
  • Myeloproliferative Disorders
  • Neoplasm Proteins
  • Protein Processing, Post-Translational

abstract

  • The discovery of mutations activating JAK-STAT signaling in the majority of patients with myeloproliferative neoplasms (MPNs) led to identification of tyrosine kinase activation as a predominant mechanism driving MPN pathogenesis. Despite this, the existence of additional genetic events that modify the MPN phenotype, predate JAK2 mutations, and/or contribute to leukemic transformation of MPNs has been suggested. Recently, mutations in several epigenetic modifiers have been described in patients with MPNs, including mutations in ASXL1, DNMT3A, EZH2, IDH1, IDH2, and TET2. Moreover, the mutant JAK2 itself has been shown recently to affect histone posttranslational modifications directly. Here we review the biological and clinical implications of epigenetic alterations in the pathogenesis of MPNs.

publication date

  • December 2013

Research

keywords

  • Review

Identity

Language

  • eng

PubMed ID

  • 24319229

Additional Document Info

start page

  • 538

end page

  • 44

volume

  • 2013