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SUMMARY:Alkis Seraphim Lecture 2018 - PI 3-Kinase and Cancer Metabolism - 
 Dr Lew Cantley
DTSTART:20181015T160000Z
DTEND:20181015T170000Z
UID:TALK110095@talks.cam.ac.uk
CONTACT:45561
DESCRIPTION:Phosphoinositide 3-Kinase (PI3K) is activated by insulin and o
 ther growth factors to mediate cell growth. The PI3K enzyme encoded by the
  PIK3CA gene is one of the most frequently mutated oncogenes in human canc
 er. This same enzyme mediates insulin responses in liver\, muscle\, fat an
 d other tissues. The most common mutations in this gene enhance the abilit
 y of PI3K to be activated by insulin.  Mosaic mutations in PIK3CA during d
 evelopment are the cause of a variety of localized overgrowth syndromes ca
 lled PROS\, in which glucose uptake and anabolic metabolism is dramaticall
 y enhanced.  The observation that PIK3CA mutations enhance responses to in
 sulin raises the possibility that elevated levels of serum insulin could d
 rive the growth of tumors that express the insulin receptor. PI3K inhibito
 rs that target PIK3CA are in clinical trials and have the expected physiol
 ogical effect of raising serum glucose and insulin levels. The elevated se
 rum insulin has the potential to reactivate PI3K in the tumor\, potentiall
 y explaining why PI3K inhibitors are not as effective as expected in treat
 ing cancers with PIK3CA mutations.  Data will be presented showing that di
 etary and pharmaceutical interventions that limit elevation of serum insul
 in improve responses to PI3K inhibitors in mouse models of cancer.  The ro
 le of PI3K in driving anabolic metabolism will also be discussed.
LOCATION:Department of Biochemistry\, Sanger Building Jean Thomas Lecture 
 Theatre
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