Dec 14, 2015
from 04:15 PM to 05:15 PM
|Where||Max Perutz Lecture Theatre, MRC Laboratory of Molecular Biology|
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In general cancer cells produce higher levels of reactive oxygen species (ROS) than normal cells due to increased rates of metabolism and defective mitochondria. In order to survive under conditions of high ROS , cancer cells typically turn on pathways for generating NADPH and glutathione to bring ROS levels back to homeostasis. Activating mutations in PIK3CA or loss of PTEN or activating mutations in KRAS can stimulate glucose uptake and metabolism and pathways for generating NADPH and glutathione to suppress ROS . A detailed understanding of the biochemical mechanisms by which cancer cells suppress excess ROS may suggest new therapies for inducing synthetic lethality in tumors that evolve in specific mutational backgrounds. Our research using human cancer cell lines and genetically engineered mouse models suggests new approaches for killing cancer cells by targeting metabolic pathways for ROS suppression that allow cancer cells to survive.
Speaker: Lewis Cantley, Meyer Cancer Center, Weill Cornell Medicine and New York Presbyterian Hospital, New York