Myelofibrosis in 2019: moving beyond JAK2 inhibition.

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2019
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Abstract
Myelofibrosis (MF) is a myeloproliferative neoplasm characterized by ineffective clonal hematopoiesis, splenomegaly, bone marrow fibrosis, and the propensity for transformation to acute myeloid leukemia. The discovery of mutations in JAK2, CALR, and MPL have uncovered activated JAK-STAT signaling as a primary driver of MF, supporting a rationale for JAK inhibition. However, JAK inhibition alone is insufficient for long-term remission and offers modest, if any, disease-modifying effects. Given this, there is great interest in identifying mechanisms that cooperate with JAK-STAT signaling to predict disease progression and rationally guide the development of novel therapies. This review outlines the latest discoveries in the biology of MF, discusses current clinical management of patients with MF, and summarizes the ongoing clinical trials that hope to change the landscape of MF treatment.
Reference Key
schieber2019myelofibrosisblood Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Schieber, Michael;Crispino, John D;Stein, Brady;
Journal blood cancer journal
Year 2019
DOI
10.1038/s41408-019-0236-2
URL
http://link.springer.com/article/10.1038/s41408-019-0236-2
Keywords
epigenetic mutations jak–stat myelofibrosis splicing

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