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SUMMARY:Targeting the brain tumour stem cell phenotype with small molecule
 s - Heiko Wurdak (Leeds)
DTSTART:20141027T160000Z
DTEND:20141027T170000Z
UID:TALK53960@talks.cam.ac.uk
CONTACT:Florian Markowetz
DESCRIPTION:Brain cancer patients with glioblastoma multiforme have a very
  poor prognosis with an average life expectancy of only 12 to 17 months. T
 hese tumours are heterogeneous and extremely difficult to treat due to tum
 our cell invasion of healthy brain tissue and resistance of the malignant 
 cells to conventional therapy. The cellular aggressiveness within brain tu
 mours has been attributed to a subpopulation of tumour cells that possess 
 stem cells-like features. Unlike differentiated tumour cells\, so called g
 lioma stem cells (GSCs) possess the ability to give rise to new tumour mas
 s from few if not single cells after surgical debulking of the tumour. The
  molecular mechanisms underlying this malignant growth are poorly understo
 od and we have used functional genomics to identify critical factors (i.e.
  TRRAP) that maintain GSCs in an undifferentiated and tumourigenic state.\
 nThe evolving notion of cancer cell heterogeneity has important implicatio
 ns for GSC-directed therapy. We investigate the plasticity of the ‘stemn
 ess’ phenotype in the context of small molecule-induced differentiation 
 and apoptosis. For example\, we analyzed GSC fate upon treatment with the 
 small molecule KHS101 using a panel of molecularly distinct GSC lines that
  were derived from clinically diverse patient tumours. The small molecule 
 KHS101 induces autophagic cell death in GSCs and eradicates the GSC phenot
 ype in a dose-dependent fashion by down-regulating the expression of GSC m
 aintenance factors (i.e. NOS2). Overall\, our data suggest that KHS101 is 
 a potential therapeutic option for the treatment of primary and recurrent 
 GBM.
LOCATION:CRUK CI Lecture Theatre
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