Clinical and molecular correlates of JAK-inhibitor therapy failure in myelofibrosis: long-term data from a molecularly annotated cohort
James T. England, Caroline McNamara, Theodore A. Kennedy, José‐Mario Capo‐Chichi, Jingyue Huang, Andrea Arruda, Taylor Nye, Verna Cheung, Jaime O. Claudio, Dawn Maze, Hassan Sibai, Anne Tierens, Hubert Tsui, Aniket Bankar, Wei Xu, Tracy Stockley, Vikas Gupta
Abstract
Myelofibrosis (MF) is an acquired clonal hematopoietic stem cell disorder associated with debilitating constitutional symptoms, extramedullary hematopoiesis resulting in splenomegaly, and a propensity to transform to a blast phase/acute myeloid leukemia (AML). The discovery of JAK inhibitors (JAKi) has been pivotal in the treatment of symptomatic MF by reducing spleen size, and alleviating cytokine-related symptom burden Despite this, up to 50% of MF patients discontinue JAKi by 2-3 years and only one quarter of patients remain on treatment at 5 years