COLONCAN

Targeting downstream effectors of Wnt signaling in colorectal cancer

Coordinatore	The Beatson Institute for Cancer Research    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	1˙499˙044 €
EC contributo	1˙499˙044 €
Programma	FP7-IDEAS-ERC Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	ERC-2012-StG_20111109
Funding Scheme	ERC-SG
Anno di inizio	2012
Periodo (anno-mese-giorno)	2012-11-01   -   2017-10-31

 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: +44 141 330 6211 Fax: +44 141 330 2899	UK (GLASGOW)	hostInstitution	1˙499˙044.80
2	The Beatson Institute for Cancer Research  Organization address address: "GARSCUBE ESTATE, SWITCHBACK ROAD" city: GLASGOW postcode: G61 1BD contact info Titolo: Prof. Nome: Owen James Cognome: Sansom Email: send email Telefono: +44 141 330 3953 Fax: +44 141 330 2899	UK (GLASGOW)	hostInstitution	1˙499˙044.80

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 Obiettivo del progetto (Objective)

'Colorectal cancer (CRC) is one of the most common cancers of the western world. The underlying initiating mutation for the majority of CRC is within the Adenomatous Polyposis Coli (Apc) gene. The APC protein performs an important role in controlling the levels of Wnt signalling by targeting beta-catenin for degradation. Loss of the APC protein leads to the activation of Wnt signaling target genes such as c-Myc which is required for phenotypes causes by Apc loss. However, despite the clear importance of APC loss and deregulated Wnt signalling, additional events are required for the development of CRC such as KRAS and P53 mutations.The impact of these changes on the development of CRC and response to therapy is not well understood. Furthermore, identification and testing of potential novel targets and therapies is hampered by lack of a preclinical model that faithfully recapitulates the course of the human disease. This proposal has two aims: 1. Assess the impact of cooperating mutations with Apc and assess how they alter sensitivities of Apc deficient cells. 2. Develop mouse models of invasive and metastatic colorectal cancer that recapitulate the human disease. We will use ‘state of the art’ methodologies to identify the changes in signaling output conferred by these cooperating mutations. Genetic mouse models of invasive and metastatic colorectal cancers will be generated through the acquisition of additional mutations and genomic instability. These studies will produce predictions on therapeutic combinations that will be tested in mouse models in vitro and in vivo that may identify new treatment regimens for patients with late stage CRC.'