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SUMMARY:MYC and Metabolic Vulnerabilities of Cancer - Chi Van Dang\, MD\, 
 PhD\, Professor and Director\, Abramson Cancer Center\, University of Penn
 sylvania Perelman School of Medicine
DTSTART:20170525T120000Z
DTEND:20170525T130000Z
UID:TALK67646@talks.cam.ac.uk
CONTACT:Kate Davenport
DESCRIPTION:The MYC oncogene\, which encodes a master transcriptional regu
 lator of proliferative metabolism\, is commonly deregulated in human cance
 rs.  Genomics studies of MYC reveal its genome-wide effect on transcriptio
 n by relieving RNA polymerase pausing.  MYC’s expression in normal cells
  is tightly regulated such that growth factor withdrawal or nutrient depri
 vation  silence MYC expression\, keeping normal cells in a non-proliferati
 ve state.  By contrast\, cancer cells with deregulated MYC undergo a force
 d program of growth\, due to MYC’s induction of ribosome biogenesis and 
 macromolecular synthesis\, which renders these cells addicted to nutrients
  to support a 'run-away' program of cell growth and proliferation.  As suc
 h\, withdrawal of nutrients or interruption of specific metabolic pathways
  with inhibitors could curb MYC-induced cancer development.  Most recently
 \, MYC was found to disrupt the circadian clock transcriptional network an
 d circadian metabolism\, presumably to allow unrestrained metabolism that 
 supports growth of a MYC-driven cancer cell.  It is also uncovered in unpu
 blished work that MYC induces a previously unsuspected rapidly oscillation
  of intracellular metabolites that could result from hyper-coupling of met
 abolic oscillators.\n\n
LOCATION:CRUK CI Lecture Theatre
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