Journal
HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA
Volume 31, Issue 4, Pages 613-+Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.hoc.2017.04.002
Keywords
JAK2V617F mutation; Myeloproliferative neoplasms; JAK2 inhibitors; JAK-STAT signaling; Myelofibrosis; Polycythemia vera; Mutant calreticulin
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Funding
- NIH [R01HL131835, K12CA087723-14]
- Damon Runyon clinical investigator award
- Starr Cancer Consortium
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Following the discovery of the JAK2V617F mutation, Janus kinase (JAK) 2 inhibitors were developed as rationally designed therapy in myeloproliferative neoplasms (MPNs). Although JAK2 inhibitors have clinical efficacy in MPN, they are not clonally selective for the JAK2V617F-mutant cells. Because activated JAK-signal transducer and activator of transcription (STAT) signaling is a common feature of MPN, JAK2 inhibitors are efficacious regardless of the specific MPN phenotypic driver mutation. The Food and Drug Administration approved the JAK1/JAK2 inhibitor, ruxolitinib, for the treatment of myelofibrosis and polycythemia vera. Additional JAK2 inhibitors are currently in advanced phased clinical trials.
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