Enhanced Molecular Response in Myeloproliferative Neoplasms with Complete JAK2V617F Inhibition

Cancer Discov. 2024 May 1;14(5):701-703. doi: 10.1158/2159-8290.CD-23-1522.

Abstract

Dunbar, Bowman, and colleagues present here a novel genetic mouse model with inducible and reversible expression of the JAK2V617F mutation in the endogenous locus. Results from this study clearly demonstrate an absolute requirement for myeloproliferative neoplasm-initiating cells for this mutation in their survival and imply that more efficacious inhibitors could be curative for these patients even in the setting of additional cooperating mutations. See related article by Dunbar et al., p. 737 (8).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Disease Models, Animal
  • Humans
  • Janus Kinase 2* / antagonists & inhibitors
  • Janus Kinase 2* / genetics
  • Mice
  • Mutation
  • Myeloproliferative Disorders* / drug therapy
  • Myeloproliferative Disorders* / genetics
  • Protein Kinase Inhibitors / pharmacology
  • Protein Kinase Inhibitors / therapeutic use

Substances

  • Janus Kinase 2
  • Protein Kinase Inhibitors