EPITHELIALSENESCENCE

Identification of Genes Controlling Senescence in Human Epithelial Cells: Role in Cancer

 Coordinatore IMPERIAL COLLEGE OF SCIENCE, TECHNOLOGY AND MEDICINE 

 Organization address address: SOUTH KENSINGTON CAMPUS EXHIBITION ROAD
city: LONDON
postcode: SW7 2AZ

contact info
Titolo: Ms.
Nome: Palalic
Cognome: Tatjana
Email: send email
Telefono: +44 20 7594 3866
Fax: +44 20 7594 3868

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 171˙740 €
 EC contributo 171˙740 €
 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-2009-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-04-01   -   2013-03-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    IMPERIAL COLLEGE OF SCIENCE, TECHNOLOGY AND MEDICINE

 Organization address address: SOUTH KENSINGTON CAMPUS EXHIBITION ROAD
city: LONDON
postcode: SW7 2AZ

contact info
Titolo: Ms.
Nome: Palalic
Cognome: Tatjana
Email: send email
Telefono: +44 20 7594 3866
Fax: +44 20 7594 3868

UK (LONDON) coordinator 171˙740.80

Mappa


 Word cloud

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replicative    expression    senescence    prostate    cancer    tumour    human    tumours    cells    epithelial    oncogenes    genes    bypass    hprecs   

 Obiettivo del progetto (Objective)

'Cellular senescence was originally described as the cell cycle arrest that accompanies the exhaustion of replicative potential in cultured primary mammalian cells. Whereas ‘replicative’ senescence is triggered by telomere erosion, other stimuli such as activated oncogenes, oxidative stress, DNA damage and sub-optimal culture conditions can also induce a senescent phenotype called ‘premature’ senescence or ‘stasis’. Senescence acts as a potent antitumor mechanism. Malignant transformation occurs after the bypass of senescence caused by mutations in oncogenes and tumour suppressors. Thus, novel genes linked with oncogenesis can be isolated by identifying genes regulating senescence. As the majority of solid tumours arise from cells of epithelial origin, the aim of the current project is to identify genes controlling senescence in epithelial cells. Specifically, human prostate epithelial cells (HprECs) will be studied as the corresponding prostate cancer represents the most frequent cancer amongst men. A genetic screening for senescence bypass will be performed in these cells using a retroviral shRNA library. The validated genes will be prioritized thanks to a parallel microarray based-analysis of transcriptional changes associated with senescence in HPrECs and to existing databases that evaluate expression profiles in human tumours. The expression of the relevant candidates will be then confirmed in a wider and independent subset of clinical tumour samples using tissue micro-array. Finally, the oncogenic properties of the candidate genes will be analysed in several models of tumourigenesis. Overall, the investigation described here aims at using senescence as a system to identify novel tumour suppressor genes.'

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