Janus kinase inhibition and its effect upon the therapeutic landscape for myelofibrosis: from palliation to cure?

Br J Haematol. 2012 May;157(4):426-37. doi: 10.1111/j.1365-2141.2012.09108.x. Epub 2012 Mar 29.


Following the discovery of the Janus kinase (JAK) 2 V617F mutation in 2005 the explosion of research and drug development activity has not only advanced our understanding of the pathogenesis of myeloproliferative neoplasms (MPNs) but also triggered debate about classification, allowed revised diagnostic and response criteria, provided a target for treatment and a mode of monitoring its success. These changes and the resultant clinical research are discussed in this article where we argue that discovery of the JAK2 V617F mutation has signalled the much delayed change in therapeutic paradigm for myelofibrosis and possibly other MPNs from palliation and allowing us to move closer to, but not yet attain, a cure.

Publication types

  • Review

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Humans
  • Janus Kinase 2 / antagonists & inhibitors
  • Janus Kinase 2 / genetics
  • Janus Kinases / antagonists & inhibitors*
  • Janus Kinases / genetics
  • Mutation
  • Myeloproliferative Disorders / drug therapy
  • Myeloproliferative Disorders / enzymology
  • Palliative Care
  • Primary Myelofibrosis / drug therapy*
  • Primary Myelofibrosis / enzymology*
  • Primary Myelofibrosis / genetics
  • Protein Kinase Inhibitors / therapeutic use*


  • Antineoplastic Agents
  • Protein Kinase Inhibitors
  • Janus Kinase 2
  • Janus Kinases