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Inhibiting oncogenic kinases to target metabolism in AML

Aaron David Schimmer

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Canadian Institutes of Health Research (CIHR)
Acute myeloid leukemia (AML) is an aggressive blood cancer. The majority of patients with AML still die from their disease and therapy for this condition is essentially unchanged in the last 20 years. Even though we have learned more about the genetic abnormalities of AML, it has proven difficult to directly target these genetic mutations. Here, we propose to target a downstream effect of these genetic mutations - cell metabolism. Recently, we demonstrated that AML cells are unique in the metabolic requirements and their dependence on a form of energy production called oxidative metabolism. We also recently demonstrated that AML but not normal cells can be killed by inhibiting protein synthesis in the mitochondria and blocking oxidative metabolism. In this proposal, we will investigate the regulation of metabolism in AML. Specifically, we will address the role of kinases and their inhibitors in affecting metabolism in AML. The results from this work will highlight a unique strategy to shift the metabolic profile of a cancer cell. By shifting the metabolic profile, we can make the AML cells vulnerable to inhibitors of oxidative metabolism and inhibitors of mitochondrial protein synthesis. Thus, our work will highlight a new therapeutic strategy for AML that could be tested rapidly in the clinic.

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