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SUMMARY:The role of aneuploidy in tumorigenesis.  - Professor Angelika Amo
 n\, MIT\, Department of Biology\, Cambridge\, MA\, USA 
DTSTART:20201022T130000Z
DTEND:20201022T140000Z
UID:TALK150559@talks.cam.ac.uk
CONTACT:Caroline Newnham
DESCRIPTION:RAD21 is a driver of chromosome 8 gain in Ewing sarcoma to enh
 ance DNA repair\n\nMarianna Trakala\, Xiaofeng A. Su and Angelika Amon\n\n
 David H. Koch Institute for Integrative Cancer Research\, Howard Hughes Me
 dical Institute\, Massachusetts Institute of Technology\, Cambridge\, MA 0
 2139.\n\nAneuploidy\, defined as whole chromosome gain or loss\, causes ce
 llular stress but\, paradoxically\, is a frequent occurrence in cancers. W
 hether or not aneuploidy contributes to tumorigenesis is however controver
 sial\, with some mouse models of chromosome instability being tumor prone 
 but others not. We investigated the role of aneuploidy in tumorigenesis an
 d found that it causes tumorigenesis with high penetrance when aneuploidy 
 levels are sufficiently high in organisms. Furthermore\, we examined the b
 asis for recurrent aneuploidies in cancer. For example\, 50% of Ewing sarc
 omas\, a pediatric bone and soft tissue tumor driven by the EWS-FLI1 fusio
 n oncogene harbor chromosome 8 gains. We investigated why this is the case
 . We found that trisomy 8 enhances repair of EWS-FLI1 induced DNA damage t
 hrough gain of a copy of RAD21\, thereby improving proliferation of EWS-FL
 I1 expressing cells. Our data further indicate that RAD21 acts within a na
 rrow\, low level overexpression range to promote tumorigenesis. We propose
  that RAD21 is the founding member of a new class of tumorigenesis promoti
 ng genes. Such genes may drive recurrent aneuploidies in cancer. \n
LOCATION:Zoom meeting
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