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Invited Commentary
May 2018

Improved JAK Inhibition in Myelofibrosis—The Long Road Ahead

Author Affiliations
  • 1Section of Hematology, Department of Internal Medicine, Yale University, and the Yale Cancer Center, New Haven, Connecticut
JAMA Oncol. 2018;4(5):659-660. doi:10.1001/jamaoncol.2017.5802

Whoever strives with all his might, that man we can redeem.

J. W. von Goethe, Faust1

Myelofibrosis (MF) is characterized by bone marrow fibrosis, extramedullary hematopoiesis and abnormal cytokine expression, which often manifest with severe splenomegaly, crippling constitutional symptoms and cytopenias.2 The identification of the Janus kinase 2 (JAK2) V617F mutation and the subsequent approval of ruxolitinib for the treatment of intermediate-risk and high-risk MF by the US Food and Drug Administration (FDA) in 2011 changed the therapeutic landscape in MF.2 Ruxolitinib effectively reduced splenomegaly and improved constitutional symptoms and quality of life in patients with intermediate-2 or high International Prognostic Scoring System risk compared with placebo or best available therapy (BAT) in the randomized phase 3 COMFORT I and COMFORT II trials, respectively.2

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