CANCER SIGNALLING

Identification and characterization of novel EGFR interactors and their implication in cancer signalling

 Coordinatore UNIVERSITY COLLEGE LONDON 

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Ms.
Nome: Malgorzata
Cognome: Kielbasa
Email: send email
Telefono: +44 2 031083064
Fax: +44 2 078132849

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 221˙606 €
 EC contributo 221˙606 €
 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-2013-IIF
 Funding Scheme MC-IIF
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-03-10   -   2016-03-09

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITY COLLEGE LONDON

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Ms.
Nome: Malgorzata
Cognome: Kielbasa
Email: send email
Telefono: +44 2 031083064
Fax: +44 2 078132849

UK (LONDON) coordinator 221˙606.40

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

cell    cancer    receptor    signalling    screens    cells    egfr    perform    erbb   

 Obiettivo del progetto (Objective)

'One of the major challenges of modern molecular biology is to understand how healthy cells transform into malignant, proliferating cells leading to diseases such as cancer and which proteins trigger these aberrant signalling cascades. The ErbB family of receptor tyrosine kinases (RTKs) are pivotal mediators of the signalling network that transmit extracellular signals into the cell and control cell growth, proliferation, differentiation and survival. Excessive ErbB signalling arises from receptor overexpression or mutation and is a hallmark of various cancers. Yet, despite 25 years of in-depth studies of RTK signalling, some aspects remain elusive and deeper understanding of signalling pathways downstream of mutant receptors will likely improve current EGFR-targeted therapies. Hence, the main aim of this proposal is to identify novel players in EGFR signalling as potential novel cancer drug targets. This will be achieved by transferring a novel two-hybrid technique that I have developed during my previous postdoc to the host institution and combining it with their expertise in cancer signalling. I will a) perform interaction screens to identify novel interactors of EGFR and its cancerous variants and b) perform small molecule compound screens to identify drugs that can interfere with interactions that specifically occur with these oncogenic EGFRs. Our ultimate goal is to identify chemical compounds that can be taken further to therapeutic development.'

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