JAK2 mutations and clinical practice in myeloproliferative neoplasms

Research output: Contribution to journalReview article

28 Scopus citations

Abstract

With the discovery in the last 3 years of novel Janus kinase 2 (JAK2) and thrombopoietin receptor (MPL) mutations, the pathogenetic understanding of and clinical practice for myeloproliferative neoplasms (MPNs) have entered a new era. Each one of these newly discovered mutations, including JAK2V617F, MPLW515L, and a JAK2 exon 12 mutation, has been shown to result in constitutive activation of JAK-STAT signaling and also induce a MPN phenotype in mice. Thus, JAK2 is now considered to be a legitimate target for drug development in MPNs, and small molecule JAK2 inhibitors have already gone through successful preclinical testing, and early-phase human trials in primary myelofibrosis have already begun. Furthermore, JAK2 mutation screening has now become a front-line diagnostic test in the evaluation of both "erythrocytosisĝ" and thrombocytosis and the 2001 World Health Organization diagnostic criteria for polycythemia vera, essential thrombocythemia, and primary myelofibrosis have now been revised to incorporate JAK2V617F mutation screening.

Original languageEnglish (US)
Pages (from-to)366-371
Number of pages6
JournalCancer Journal
Volume13
Issue number6
DOIs
StatePublished - Nov 1 2007

Keywords

  • Essential thrombocythemia
  • Exon 12
  • JAK2
  • JAK2-V617F
  • JAK2V617F
  • MPL
  • Mutation
  • Myelofibrosis
  • Myeloproliferative
  • Polycythemia

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Fingerprint Dive into the research topics of 'JAK2 mutations and clinical practice in myeloproliferative neoplasms'. Together they form a unique fingerprint.

  • Cite this