KIDNEY CANCER

Molecular mechanisms underlying control of renal epithelial proliferative homeostasis

 Coordinatore  

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore Non specificata
 Totale costo 1˙500˙000 €
 EC contributo 1˙500˙000 €
 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-2010-StG_2009111
 Anno di inizio 2010
 Periodo (anno-mese-giorno) 2010-12-01   -   2015-11-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITAET ZUERICH

 Organization address address: Raemistrasse 71
city: ZURICH
postcode: 8006

contact info
Titolo: Prof.
Nome: Ian James
Cognome: Frew
Email: send email
Telefono: +41 44 635 50 04
Fax: +41 44 635 68 14

CH (ZURICH) hostInstitution 1˙500˙000.00

Mappa


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expression    genetic    kidney    molecular    interference    cell    experimental    mouse    therapeutic    ccrcc    libraries    gene    rna    time    first    grant    serve   

 Obiettivo del progetto (Objective)

'This research grant has two major aspects. The first seeks to understand the molecular and cellular basis of the evolution of clear cell renal cell carcinoma(ccRCC), the most frequent form of kidney cancer. We will utilise an integrated approach based on mouse genetics, the use of primary kidney epithelial cell culture systems, genetic screening approaches using RNA interference libraries and analysis of the genetic and molecular changes that arise in human kidney tumours. The rationale behind these studies is that by better understanding the molecular causes of ccRCC it will be possible to identify new molecules or signaling pathways that could serve as appropriate therapeutic targets. The second aspect of this grant relates to the development of a flexible experimental platform that will allow the rapid and simultaneous up- and down-regulation of gene expression in the mouse kidney in a manner in which the affected cells are marked by a luminescent marker. This system will be based on the injection of modified lentiviral gene overexpression and gene knockdown vectors, allowing us to exploit recently-developed genome-wide cDNA libraries and RNA interference libraries. This experimental system should be equally applicable to other organ systems and will allow for the first time a systematic approach to the manipulation of gene expression in living mice, additionally bypassing the time limitations associated with conventional mouse genetic approaches. We aim to develop this system within the biological context of this grant and will combine it with live-animal imaging approaches to generate a series of mouse models of ccRCC. These will ultimately serve as invaluable tools for testing novel therapeutic approaches against this currently untreatable disease.'

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