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New therapies and gene target advance the treatment and understanding of hard-to-treat leukemias
Date:12/6/2010

tion who failed both imatinib and nilotinib therapy achieved a complete hematologic response and a complete cytogenetic response with ponatinib. Overall, 13 out of 60 patients (22 percent) with Ph+ disease achieved a major molecular response, including 12 out of 42 patients (28 percent) with CML in chronic phase and six out of 15 patients (40 percent) with T315I mutation confirmed at the start of the study. Twelve major molecular responses occurred in patients who received ponatinib for four months or less. There were four major molecular responses in patients who received ponatinib for only two months or less. Major molecular responses also were seen in patients with the following mutations: M351T, F359C, F317L, M244V, and G250E.

"These results are exciting because it is very difficult to induce responses, particularly at the high rates seen with ponatinib, in heavily refractory patients," said lead study author Jorge Cortes, MD, Deputy Chair and Professor of Medicine, Department of Leukemia, The University of Texas MD Anderson Cancer Center in Houston. "While these results need to be confirmed in a larger study, ponatinib may be the next step in coming closer to overcoming, and possibly preventing, the most difficult mechanisms of resistance in CML, and ultimately finding a cure for Philadelphia chromosome-positive leukemias."

Dr. Cortes will present this study in an oral presentation on Monday, December 6, at 7:00 a.m. in Room Valencia A.

Impaired Hydroxylation of 5-Methylcytosine in TET2 Mutated Patients With Myeloid Malignancies [Abstract 1]

In previous research, mutations in the TET2 (Ten-Eleven Translocation-2) gene were found across a broad range of myeloid malignancies, but little is known about the pathologic consequences of this mutation or the role it plays in the development of diseases such as myelo
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Contact: Lindsey Love
llove@hematology.org
540-538-9326
American Society of Hematology
Source:Eurekalert

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