PANCREATIC CANCER

Pancreatic stellate cells - sentinels for tissue damage?

 Coordinatore 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

 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

Mappa


 Word cloud

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anti    pancreas    cells    pda    function    tumour    psc    stellate    pancreatic   

 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.'

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