Turn It Off! Genetic Switch System Suggests Targeting of Mutant JAK2 Reverses Myeloproliferative Neoplasms
Author:
Affiliation:
1. MRC Weatherall Institute of Molecular Medicine, University of Oxford, U.K.
Publisher
American Society of Hematology
Reference7 articles.
1. JAK-STAT pathway activation in malignant and nonmalignant cells contributes to MPN pathogenesis and therapeutic response;Kleppe;Cancer Discov,2015
2. Long-term findings from COMFORT-II, a phase 3 study of ruxolitinib vs best available therapy for myelofibrosis;Harrison;Leukemia,2016
3. The effect of long-term ruxolitinib treatment on JAK2p.V617F allele burden in patients with myelofibrosis;Deininger;Blood,2015
4. Challenges and perspectives for therapeutic targeting of myeloproliferative neoplasms;Brkic;Hemasphere,2020
5. Distinct roles for long-term hematopoietic stem cells and erythroid precursor cells in a murine model of Jak2V617F-mediated polycythemia vera;Mullally;Blood,2012
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