INFECTIONCANCER

Identifying genetic and microbial factors that promote intestinal inflammation and cancer using Drosophila

 Coordinatore UNIVERSITY OF CYPRUS 

 Organization address address: KALLIPOLEOS STREET 75
city: NICOSIA
postcode: 1678

contact info
Titolo: Mr.
Nome: Evis
Cognome: Drousiotis
Email: send email
Telefono: +357 22 894296

 Nazionalità Coordinatore Cyprus [CY]
 Totale costo 100˙000 €
 EC contributo 100˙000 €
 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-2011-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-05-01   -   2016-04-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITY OF CYPRUS

 Organization address address: KALLIPOLEOS STREET 75
city: NICOSIA
postcode: 1678

contact info
Titolo: Mr.
Nome: Evis
Cognome: Drousiotis
Email: send email
Telefono: +357 22 894296

CY (NICOSIA) coordinator 100˙000.00

Mappa


 Word cloud

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inflammatory    drosophila    signalling    host    cancer    predispose    bacterial    human    intestinal    inflammation    disease    pathways   

 Obiettivo del progetto (Objective)

'My long term goal is to establish a network of bacterial factors and the host signalling pathways they modulate in wild type and mutated intestinal cells that predispose for inflammation and cancer. The work of my future team will ultimately lead to a deeper understanding of critical aspects of intestinal human disease, including inflammatory bowel disease and the intestinal tumor formation and metastasis. To rapidly assess numerous combinations of inflammatory and anti-inflammatory host genes, bacterial species and their excreted factors we will use in this proposal Drosophila genetics and transcriptome analysis, chemical treatments and microbiological assays to identify the host and microbial factors that mediate inflammation and predispose for cancer using Drosophila. Despite the physiological divergence that exists between vertebrates and insects, modelling of human diseases is possible because of the high degree of conservation between Drosophila and mammalian signalling pathways controlling inflammation and infection.'

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