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SUMMARY:Milstein Lecture-Phosphoinositide 3-Kinase and Cancer Metabolism -
  Lewis Cantley\, Meyer Cancer Center\, Weill Cornell Medicine and New York
  Presbyterian Hospital\, New York
DTSTART:20151214T161500Z
DTEND:20151214T171500Z
UID:TALK60116@talks.cam.ac.uk
CONTACT:Scientific Meetings Co-ordinator
DESCRIPTION:In general cancer cells produce higher levels of reactive oxyg
 en species (ROS) than normal cells due to increased rates of metabolism an
 d defective mitochondria.  In order to survive under conditions of high RO
 S\, cancer cells typically turn on pathways for generating NADPH and gluta
 thione to bring ROS levels back to homeostasis.  Activating mutations in P
 IK3CA or loss of PTEN or activating mutations in KRAS can stimulate glucos
 e uptake and metabolism and pathways for generating NADPH and glutathione 
 to suppress ROS.  A detailed understanding of the biochemical mechanisms b
 y which cancer cells suppress excess ROS may suggest new therapies for ind
 ucing synthetic lethality in tumors that evolve in specific mutational bac
 kgrounds.  Our research using human cancer cell lines and genetically engi
 neered mouse models suggests new approaches for killing cancer cells by ta
 rgeting metabolic pathways for ROS suppression that allow cancer cells to 
 survive.
LOCATION:Max Perutz Lecture Theatre\, Medical Research Council (MRC) (MRC 
 Laboratory of Molecular Biol
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