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Mount Sinai School of Medicine
Translational Regulation of Gene Expression in Acute Myelogenous Leukemia (AML)
Dr. Sternberg’s laboratory is committed to the development of therapeutic strategies for leukemia through knowledge of aberrant information signaling within the cancer cell. The generation of leukemias is caused in many instances by mutation of rogue oncogenes that disrupt normal cell signaling. Two of these, the NPM and FLT3 genes, are among the most commonly mutated targets in patients with acute myelogenous leukemia (AML).
In this effort Dr. Sternberg’s team is exploring the mechanism of leukemia induction by the mutant NPM and FLT3 gene products. In particular, they focus on the conversion of genetic information in the form of messenger RNA into abnormal protein expression. Their hypothesis is that mutant NPM and FLT3 usurp this process, termed translation, in patients with AML. They are using state-of-the-art gene expression profiling technologies to understand how mutant NPM and FLT3 alter normal translation within a cancer cell. Moreover, Dr. Sternberg’s team will develop models to validate the functional role of particular translational targets in the pathogenesis of AML. They anticipate that the insights gained from this study will inform new prognostic and therapeutic strategies for the treatment of these frequently lethal neoplasms.