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SUMMARY:Targeting Therapy-evading Cancer Cells in Gliomas and Pancreatic C
 ancer. - Andreas Androutsellis-Theotakis\, CEO/CSO Innate Repair and Assis
 tant Professor\, Technische Universitaet\, Dresden
DTSTART:20191127T110000Z
DTEND:20191127T120000Z
UID:TALK134548@talks.cam.ac.uk
CONTACT:Kirsty Shepherd
DESCRIPTION:Current oncology therapies face difficulties in opposing the r
 egenerative properties of cancer\; as a result\, some cancers have a very 
 low life expectancy and many cancers have a significant probability of rec
 urrence. At the cellular level\, this is largely because some cancer cells
  evade therapy and then regenerate the tumour. At the molecular level\, th
 ey do so by switching molecular growth mechanisms. When a drug designed to
  disrupt established growth mechanisms is applied\, they switch over to op
 erating an alternative mechanism (the Hes3 Signalling Axis)\, thus continu
 ing disease progression. Operation of the alternative mechanism confers st
 em cell-like qualities that may help the regeneration of the tumour. At th
 e heart of this alternative mechanism is the gene Hes3\, a transcription f
 actor that is found to be expressed in regenerating tissue and multiple ca
 ncers (including gliomas\, pancreatic and lung). In multiple types of canc
 er\, Hes3 expression correlates with reduced life expectancy. Having ident
 ified this mechanism\, we are now validating the efficacy of two types of 
 treatment at the pre-clinical stage:\n1.	A Hes3 siRNA that directly target
 s Hes3 and.\n2.	A series of FDA-approved small molecule drugs we aim to re
 purpose in oncology that in vitro specifically kill glioma cells only when
  they operate the Hes3 signalling axis.\nOptimal delivery of these treatme
 nts in the context of gliomas (to start with) is critical to the success o
 f this new therapeutic strategy.\n
LOCATION:Electrical Engineering\, Department of Engineering - EED Seminar 
 Room - 9 JJ Thomson Avenue\, Cambridge\, CB3 0FA
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