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JAK inhibitor provides rapid, durable relief for myelofibrosis patients
Date:9/15/2010

halting therapy.

"The JAK2V617F mutation is one of several involved in myelofibrosis. It's the most prevalent, found in about half of patients. But it's not the sole cause of the disease," Verstovsek noted. "Myelofibrosis is too complex to be eliminated by a single drug. It will probably take combination therapies to cure it."

Normally, JAK2 is turned on by various growth factors to make new blood cells as needed. The JAK2V617F mutation leaves the JAK2 enzyme permanently turned on, which causes the overgrowth of bone marrow cells at the heart of myelofibrosis.

While the JAK2 inhibitor was expected to help patients with JAK2 mutations, the drug worked whether they had the mutation or not. "This suggests that patients who do not have specific mutations still have a very active JAK signaling pathway and can benefit from JAK inhibition," Verstovsek said. "However, because the drug also inhibits normal JAK2, it can lead to low blood counts that can limit dosing."


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Contact: Scott Merville
smerville@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert

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