Enhanced Molecular Response in Myeloproliferative Neoplasms with Complete JAK2V617F Inhibition.
Hamza CelikGrant A ChallenPublished in: Cancer discovery (2024)
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).
Keyphrases
- mouse model
- end stage renal disease
- prognostic factors
- newly diagnosed
- induced apoptosis
- ejection fraction
- poor prognosis
- chronic kidney disease
- peritoneal dialysis
- cell cycle arrest
- rectal cancer
- gene expression
- cell proliferation
- signaling pathway
- single molecule
- long non coding rna
- high grade
- binding protein
- patient reported
- drug induced