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SUMMARY:"Strategies to enhance effectiveness of Radiotherapy in Pancreatic
  Cancer" - Dr Thomas Brunner\, Gray Institute for Radiation Oncology and B
 iology\, Oxford
DTSTART:20120515T110000Z
DTEND:20120515T120000Z
UID:TALK36345@talks.cam.ac.uk
CONTACT:Mala Jayasundera
DESCRIPTION:The molecular major characteristics of pancreatic cancer have 
 now been relatively well characterised. This enables the preclinical and c
 linical testing of the combination of molecular targeted agents in conjunc
 tion with radiotherapy. Pancreatic cancer is characterised by a high rate 
 of mutations in K-Ras (>90%) and p53 (50-75%). Inhibition of Ras as well a
 s of upstream (EGFR) and downstream pathways of Ras were tested clinically
  to enhance cytotoxicity of radiotherapy to pancreatic cancer cells. As AT
 M-signalling is suppressed in the context of K-Ras and p53 mutations\, tar
 geting of ATR/Chk1  as the activated backup pathway for DNA double strand 
 breaks appears to be an attractive strategy to be combined with radiothera
 py.  Furthermore\, pancreatic cancer is a prime example of a tumour with a
  rich stromal reaction (desmoplasia) and pancreatic stellate cells which d
 rive this reaction have been recognised to contribute to radiation resista
 nce of pancreatic cancer. The stromal reaction also contributes to the dra
 matic hypoxia found in pancreatic cancers\, one of the most important fact
 ors of radiation resistance\,  and signal transduction inhibitors of the E
 GFR/Ras/PI3 kinase/Akt pathway have been recognised to lead to a prolonged
  reoxygenation. These examples of using molecular strategies in conjunctio
 n with radiotherapy are given to reflect possible future strategies to imp
 rove outcomes.
LOCATION:CRI Lecture Theatre
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