WNT IN THE INTESTINE

Wnt Signalling in Colorectal Carcinogenesis and Intestinal Homeostasis

Coordinatore	The Beatson Institute for Cancer Research    more  Organization address address: "GARSCUBE ESTATE, SWITCHBACK ROAD" city: GLASGOW postcode: G61 1BD contact info Titolo: Mr. Nome: Peter Cognome: Winckles Email: send email Telefono: 441413000000 Fax: 441419000000
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	183˙618 €
EC contributo	183˙618 €
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	2009
Periodo (anno-mese-giorno)	2009-05-01   -   2011-04-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	The Beatson Institute for Cancer Research  Organization address address: "GARSCUBE ESTATE, SWITCHBACK ROAD" city: GLASGOW postcode: G61 1BD contact info Titolo: Mr. Nome: Peter Cognome: Winckles Email: send email Telefono: 441413000000 Fax: 441419000000	UK (GLASGOW)	coordinator	183˙618.80

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 Obiettivo del progetto (Objective)

'The intestinal epithelium is a highly self-renewing tissue, which is replenished by multipotent stem cells. Deregulation of normal intestinal homeostasis often results in malignant transformation. Colorectal carcinoma is one of the most common cancers in western world. Inactivating mutations of the Apc (Adenomatous Polyposis Coli) gene is key for colorectal cancer; up to 80% of sporadic colorectal cancers have Apc mutations. The main tumour suppressive function of Apc is to negatively regulate Wnt signalling, however the functional significance of the pathways downstream of Apc remains elusive. Furthermore, the contribution of intestinal stem cells to colorectal cancer is unclear. The host laboratory has generated a mouse model to study the acute consequences of Apc loss in vivo. Using microarray analysis the lab has identified numerous novel Wnt target genes that are up regulated at all stages of colorectal carcinogenesis. These genes may be important modifiers of the Apc phenotypes but, given their number and potential redundancies, they cannot be tested in a high throughput manner in the mouse. Drosophila melanogaster is one of the best model organisms to perform genetic screens. Recent reports have shown that the Drosophila adult gut has remarkable resemblance to the vertebrate intestine. Importantly, Drosophila intestinal stem cells have been unambiguously identified. In this proposal I will: A) Generate a Drosophila model of Apc driven gut tumourigenesis. B) Test the fly orthologues of the mouse candidate target genes in this system. C) Test the modifiers of the Drosophila phenotype in the mouse model of Apc loss. Ours is a novel approach, which takes advantage of two in vivo genetic model systems to shed light into the molecular and cellular mechanisms regulating malignant transformation within the intestinal epithelium.'