PANCREATIC CANCER

Pancreatic stellate cells - sentinels for tissue damage?

Coordinatore	CANCER RESEARCH UK    more  Organization address address: ST JOHN STREET 407 ANGEL BUILDING city: LONDON postcode: EC1V 4AD contact info Titolo: Dr. Nome: Emma Cognome: Ryley Email: send email Telefono: +44 (0) 1223 404262 Fax: +44 (0) 1224 404199
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	0 €
EC contributo	171˙300 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-IEF-2008
Funding Scheme	MC-IEF
Anno di inizio	2010
Periodo (anno-mese-giorno)	2010-01-01   -   2011-12-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	CANCER RESEARCH UK  Organization address address: ST JOHN STREET 407 ANGEL BUILDING city: LONDON postcode: EC1V 4AD contact info Titolo: Dr. Nome: Emma Cognome: Ryley Email: send email Telefono: +44 (0) 1223 404262 Fax: +44 (0) 1224 404199	UK (LONDON)	coordinator	171˙300.62

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 Obiettivo del progetto (Objective)

'Pancreatic ductal adenocarcinoma (PDA) is a lethal disease killing about 7000 people in the United Kingdom every year. PDA is resistant to conventional therapy. A hallmark of PDA is the abundance of desmoplastic stroma, which is thought to originate by activation of pancreatic stellate cells (PSC). Unfortunately, little is know about the precise role of PSC in the physiology of the pancreas. In this proposal I will investigate the function of the pancreatic stellate cell in health and during tumour development using a murine model of PDA. I hypothesize, that PSC function as antigen-presenting cells surveying the microenvironment for tissue damage. I postulate, that PSC induce repair processes as well as immunosuppressive responses by means of retinoic acid signalling (PSC are a major vitamin A storage) and the secretion of TGFbeta. This anti-inflammatory program may serve to prevent the autoimmune destruction of the pancreas, an organ indispensable for survival. However, during cancer development this default program may be detrimental as it inhibits the mounting of a proper anti-tumour response.'