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SUMMARY:Innate Genetics and the Tumour Microenvironment Cooperate to Drive
  Prostate Cancer Aggression - Prof Robert G Bristow\, Senior Scientist\, P
 rincess Margaret Cancer Centre\, Toronto
DTSTART:20160223T120000Z
DTEND:20160223T130000Z
UID:TALK62042@talks.cam.ac.uk
CONTACT:Mala Jayasundera
DESCRIPTION:Prostate cancer (CaP) remains the most common male malignancy 
 worldwide. Although some localized cancers can be indolent\, others can ma
 nifest aggressive biology with abnormal cancer metabolism and genetic inst
 ability. These men need intensified treatment to prevent metastatic castra
 te-resistant disease (mCRPC). We have embarked upon a broad analysis of ca
 ncer metabolism (hypoxia)\, whole-genomes and methylomes in close to 400 m
 en treated with surgery or radiotherapy to derive novel signatures of outc
 ome. Non-indolent tumours treated by surgery or radiotherapy have a paucit
 y of clinically-actionable mutations\; in distinct contrast to that report
 ed for mCRPC.  A significant proportion of tumours harbour recurrent non-c
 oding aberrations\, important genomic rearrangements\, and chromothripsis 
 or kataegis. Importantly\, this disparity in genomic landscape between oth
 erwise pathologically similar cancers explained heterogeneity in clinical 
 outcome as multiple driver mutations\, gene methylation and copy-number al
 terations are directly with aggressive disease and patient outcome. The pr
 esence of hypoxia furthers the effect of genetic instability on adverse ou
 tcome. Our data strongly suggest that novel therapeutic approaches should 
 also focus on recurrent non-mutation targets in localized prostate cancer 
 in order to improving cures in aggressive localized disease. It also provi
 des genetically disparate risk groups that can be triaged to treatment int
 ensification to improve cure.  
LOCATION:CRUK CI Lecture Theatre
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