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Myelofibrosis (MF) is thought to originate from mutations that induce development of a stem cell clone that stimulates bone marrow fibrosis (NEJM JW Oncol Hematol Sep 2014 and Blood 2014; 124:1062). Targeting specific mutations such as the V617F mutation of Janus kinase has resulted in durable remissions (NEJM JW Oncol Hematol Dec 2013 and Blood 2013; 122:4047). Another potential approach is to limit cell proliferation, which might be accomplished by inhibiting the cytoprotective enzyme telomerase.
To assess whether imetelstat, an inhibitor of telomerase and cell proliferation, has activity in patients with MF, investigators conducted an industry-sponsored pilot study involving 33 patients with advanced myelofibrosis, of whom 55% had primary…