Enhanced Molecular Response in Myeloproliferative Neoplasms with Complete JAK2V617F Inhibition

Author:

Celik Hamza1ORCID,Challen Grant A.2ORCID

Affiliation:

1. 1Incyte Research Institute, Wilmington, Delaware.

2. 2Division of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri.

Abstract

Summary: 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).

Publisher

American Association for Cancer Research (AACR)

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