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• W2994303605 abstract "Abstract The Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) share a common pathobiology of constitutive activation of the JAK and STAT pathway, despite having the 3 distinct phenotypes of essential thrombocythemia, polycythemia vera, and primary myelofibrosis. Targeting the JAK-STAT pathway has led to remarkable clinical benefit, including reduction in splenomegaly, amelioration of cytokine-driven symptoms, improvement in quality of life, and even some improvement in survival. However, targeting this pathway has not resulted in consistent disease modification by current metrics, including a reduction in mutant allele burden or reversal of fibrosis. Moreover, targeting JAK-STAT can lead to limiting treatment-emergent side effects, such as anemia and thrombocytopenia. Continued discovery points to a complex system of pathogenesis beyond JAK-STAT driving the formation and evolution of MPNs. This article reviews the successes and limitations of JAK-STAT inhibition, surveys the strategies behind emerging therapies, and discusses the challenges that are present in moving beyond JAK-STAT." @default.
• W2994303605 created "2019-12-13" @default.
• W2994303605 creator A5023728016 @default.
• W2994303605 date "2019-12-06" @default.
• W2994303605 modified "2023-09-30" @default.
• W2994303605 title "Beyond JAK-STAT: novel therapeutic targets in Ph-negative MPN" @default.
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• W2994303605 doi "https://doi.org/10.1182/hematology.2019000048" @default.
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