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SUMMARY:The Ras pathway in cancer therapy - Frank McCormick\, UCSF Helen D
 iller Family Comprehensive Cancer Center
DTSTART:20121003T120000Z
DTEND:20121003T130000Z
UID:TALK34412@talks.cam.ac.uk
CONTACT:Kate Davenport
DESCRIPTION:K-Ras genes and N-Ras are frequently activated in cancer. Atte
 mpts to develop drugs that target mutant Ras have so far been unsuccessful
 .  The reasons for these failures\, and possible solutions based on new ap
 proaches\, will be discussed. Drugs that inhibit Raf have failed to show c
 linical benefit in Ras-mutant tumors.  In contrast\, they paradoxically in
 duce the Raf MAPK pathway in these cells.  This\, we propose\,  is because
  Raf is negatively regulated by auto-phosphorylation\, so that Raf inhibit
 ors relieve auto-phosphorylation before they inhibit MEK phosphorylation. 
 \nK-Ras is activated far more frequently than N-Ras or H-Ras  in human can
 cers. K-Ras\, but not H-Ras activates a set of genes which are involved in
  stem cell phenotypes\,. K-Ras is able to promote multiple stem cell chara
 cteristics in vitro and in vivos.  These data may explain why cancer cells
  driven by K-Ras are especially difficult to treat and offer new opportuni
 ties for therapeutic intervention\n\n
LOCATION:Cancer Research UK Cambridge Research Institute\, Lecture Theatre
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