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SUMMARY:****CANCELLED***Mammalian SWI/SNF (BAF) complex structure and func
 tion in human cancer - Cigall Kadoch\, Ph.D\, Dana- Farber Cancer Institut
 e and Harvard Medical School\, Boston
DTSTART:20170615T120000Z
DTEND:20170615T130000Z
UID:TALK67647@talks.cam.ac.uk
CONTACT:Kate Davenport
DESCRIPTION:Exome- and genome-wide sequencing studies in human cancer have
  revealed a striking frequency of mutations in the genes encoding subunits
  of the mammalian SWI/SNF (BAF) family of ATP-dependent chromatin remodeli
 ng complexes. We recently determined these mutations to be broadly recurre
 nt in over 20% of all cancers. Here\, we present studies focused on BAF co
 mplex assembly and architecture\, cancer-specific complex subunit and asso
 ciated protein factor composition\, and novel approaches toward the identi
 fication of small molecule therapeutics for this class of human tumors. \n
  \nTo investigate the underlying mechanism\, our group has studied genomic
 ally well-defined cancer types driven by both gain- and loss-of-function m
 utations to genes encoding BAF complex subunit or associated factors. Thes
 e include human synovial sarcoma (SS) in which 100% of tumors have a preci
 se translocation involving the SS18 subunit\, malignant rhabdoid tumors wh
 ich are driven by deletion of the BAF47 (SMARCB1) subunit\, and more recen
 tly cancers driven by aberrant activation of transcription factors which b
 ind to and direct BAF complex targeting. Taken together\, the study of BAF
  complex-mediated oncogenesis in these disease settings has provided us wi
 th a powerful foundation upon which to understand the precise oncogenic me
 chanisms directed by altered subunit composition\, structure and function 
 of chromatin remodeling complexes.\n
LOCATION:CRUK CI Lecture Theatre
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