Hydroxyurea (HU) is effective in reducing JAK2V617F mutated clone size in the peripheral blood of essential thrombocythemia (ET) and polycythemia vera (PV) patients

Ann Hematol. 2009 Jul;88(7):629-32. doi: 10.1007/s00277-008-0650-1. Epub 2008 Dec 19.

Abstract

Ph-negative chronic myeloproliferative disorders (Ph(neg)cMPD) are treated according to the estimated vascular risk. The recent discovery of V617F point mutation of the JAK2 kinase, which frequently occurs in these diseases, has not changed their management so far. However, emerging data tend to support a prothrombotic role for the mutation, along with a better response of JAK2V617F mutated patients to hydroxyurea treatment. Our data further support this notion.

Publication types

  • Clinical Trial

MeSH terms

  • Bone Marrow
  • Clone Cells / drug effects
  • Clone Cells / pathology
  • Hematopoietic Stem Cells
  • Humans
  • Hydroxyurea / administration & dosage
  • Hydroxyurea / pharmacology*
  • Janus Kinase 2 / genetics*
  • Mutation, Missense
  • Polycythemia Vera / blood
  • Polycythemia Vera / drug therapy*
  • Polycythemia Vera / pathology
  • Thrombocythemia, Essential / blood
  • Thrombocythemia, Essential / drug therapy*
  • Thrombocythemia, Essential / pathology
  • Thrombophilia / genetics
  • Treatment Outcome

Substances

  • Janus Kinase 2
  • Hydroxyurea