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SUMMARY:&quot\;Hijacking of NMDA receptor signalling by tumors&quot\; - Pr
 ofessor Douglas Hanahan\, Swiss Institute for Experimental Cancer Research
 \, EPFL\, Lausanne\, Switzerland
DTSTART:20160509T153000Z
DTEND:20160509T170000Z
UID:TALK65123@talks.cam.ac.uk
CONTACT:Lyn Dakin
DESCRIPTION:“Linkage analysis of a polymorphic differences in the malign
 ant phenotype in a mouse model of pancreatic neuroendocrine cancer (PanNET
 ) led to a genetic modifier locus (Chun et al 2010)\, and in turn to a can
 didate gene – GKAP - contained therein.  GKAP is involved in transmittin
 g signals from the glutamate-stimulate NMDA receptor.  Evaluation of NMDAR
  revealed that signaling was activated in PanNET cancer cells\, in part by
  hydrodynamic pressure\, involving autocrine secretion of glutamate and st
 imulation of NMDAR.  Glutamate-stimulated NMDAR signaling enhanced both pr
 oliferation and invasion of PanNET cancer cells\, effects that could be am
 eliorated by prototypical inhibitors of NMDAR (Li and Hanahan 2013).  More
  recently\, we have further characterized the role of GKAP as a modulator 
 of these effects\, investigated downstream signaling\, revealing links to 
 translational control\, and extended the association to the more prevalent
  form of pancreatic cancer\, ductal adenocarcinoma.”\n\nReferences:\nChu
 n\, M.G.\, Mao\, J.H.\, Chiu\, C.W.\, Balmain\, A.\, & Hanahan\, D. (2010)
 .  Polymorphic genetic control of tumor invasion in a mouse model of pancr
 eatic neuroendocrine carcinogenesis. PNAS 107: 17268-17273.\n\nLi\, L.\, &
  Hanahan\, D. (2013). Hijacking the neuronal NMDAR signaling circuit to pr
 omote tumor growth and invasion. Cell. 153: 86-100. \n\n\n
LOCATION:The Hodgkin Huxley Seminar Room\, Department of Physiology Develo
 pment and Neuroscience
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