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Animal model demonstrates role for metabolic enzyme in acute myeloid leukemia
Date:1/28/2014

hat compound mutant animals developed acute leukemias," explains Reschke. "This exciting finding told us that mutant IDH2 contributes to leukemia initiation in vivo." As with the retroviral transduction model, genetic deinduction of mutant IDH2 in the context of a cooperating Flt3 mutation resulted in reduced proliferation and/or differentiation of leukemic cells, further demonstrating that mutant IDH2 expression is required for leukemia maintenance.

"This model has validated mutant IDH proteins as very strong candidates for continued development of targeted anticancer therapeutics," says Pandolfi. "The model will also be of paramount importance to study mechanisms of resistance to treatment that may occur."


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Contact: Bonnie Prescott
bprescot@bidmc.harvard.edu
617-667-7306
Beth Israel Deaconess Medical Center
Source:Eurekalert

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