Craig B. Thompson, MD
President and Chief Executive Officer
Memorial Sloan-Kettering Cancer Center
Proliferating cancer cells exhibit a robust but seemingly wasteful metabolism. Two nutrients, glucose and glutamine, are consumed by tumor cells at rates in vast excess of their utilization by vegetative cells. The uptake of each of these nutrients is under the control of distinct oncogenes. The PI3K/Akt/TOR signaling pathway plays the primary role in directing cellular glucose uptake and metabolism. Deregulation of this pathway in cancer can be imaged in vivo by FDG-PET scans. Recent evidence suggests that the myc family of oncogenes direct glutamine uptake and mitochondrial catabolism in transformed cells. Glutamine and glucose metabolism facilitate distinct mitochondrially-dependent synthetic reactions required for growth. Recent evidence suggests tumor suppressors are counter-regulators of mitochondrial biosynthesis. In the case of hypoxia, conversion to anaerobic glycolysis is induced by activation of HIF-1. In the case of glucose limitation, conversion to fatty acid oxidation is mediated by activation of p53. The roles of oncogenes and tumor suppressors in the regulation of metabolic pathways will be discussed. Therapeutic strategies to selectively impair tumor metabolism will be considered.
Supported by the Research Centers for Minority Institutions Program National Institutes of Health – G12-RR-03037 and grant UL1RR024996 of the CTSC at Weill Cornell Medical College.
Hunter College, Ida Lang Recital Center
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dc674 (at) hunter (dot) cuny (dot) edu