"Hijacking of NMDA receptor signalling by tumors"

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• Professor Douglas Hanahan, Swiss Institute for Experimental Cancer Research, EPFL, Lausanne, Switzerland
• Monday 09 May 2016, 16:30-18:00
• The Hodgkin Huxley Seminar Room, Department of Physiology Development and Neuroscience.

If you have a question about this talk, please contact Lyn Dakin.

“Linkage analysis of a polymorphic differences in the malignant 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 candidate gene – GKAP - contained therein. GKAP is involved in transmitting 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 stimulation of NMDAR . Glutamate-stimulated NMDAR signaling enhanced both proliferation and invasion of PanNET cancer cells, effects that could be ameliorated 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.”

References: Chun, M.G., Mao, J.H., Chiu, C.W., Balmain, A., & Hanahan, D. (2010). Polymorphic genetic control of tumor invasion in a mouse model of pancreatic neuroendocrine carcinogenesis. PNAS 107 : 17268-17273.

Li, L., & Hanahan, D. (2013). Hijacking the neuronal NMDAR signaling circuit to promote tumor growth and invasion. Cell. 153: 86-100.

This talk is part of the Adrian Seminars in Neuroscience series.

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