ALTANGIOTARGET

Understanding tumour resistance: Receptors and signalling pathways that can lead the race against tumour angiogenesis

 Coordinatore UNIVERSITY OF PATRAS 

 Organization address address: UNIVERSITY CAMPUS RIO PATRAS
city: RIO PATRAS
postcode: 26500

contact info
Titolo: Prof.
Nome: Evangelia
Cognome: Papadimitriou
Email: send email
Telefono: +30 2610969336
Fax: +30 2610969336

 Nazionalità Coordinatore Greece [EL]
 Totale costo 161˙968 €
 EC contributo 161˙968 €
 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-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2015
 Periodo (anno-mese-giorno) 2015-03-16   -   2017-03-15

 Partecipanti

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

 Organization address address: UNIVERSITY CAMPUS RIO PATRAS
city: RIO PATRAS
postcode: 26500

contact info
Titolo: Prof.
Nome: Evangelia
Cognome: Papadimitriou
Email: send email
Telefono: +30 2610969336
Fax: +30 2610969336

EL (RIO PATRAS) coordinator 161˙968.80

Mappa


 Word cloud

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

integrin    pathways    cell    vegf    resistance    migration    beta    alpha    induced    vitro    anti    signalling    gbm    endothelial    receptor    therapy    bevacizumab    receptors    angiogenesis    angiogenic    co    alternative   

 Obiettivo del progetto (Objective)

'Anti-vascular endothelial growth factor (VEGF) therapies, such as bevacizumab, inhibit VEGF angiogenic actions and are increasingly used in the clinic as anticancer regimens for a variety of tumours, among which glioblastoma multiforme (GBM), the most lethal and angiogenic brain tumour, characterized by a high degree of heterogeneity. However, resistance to anti-angiogenic therapy, which leads to ineffectiveness of the existing drugs, is often acquired and suggests that there is urgent need to identify novel targets and develop alternative or complementary therapeutic options. Previous in vitro studies of the host lab have identified a novel receptor that binds VEGF and through co-operation with alpha v beta 3 integrin, is required for VEGF-induced endothelial and GBM cell migration. This receptor also mediates VEGF effects that are not inhibited by bevacizumab, encouraging the hypothesis that its targeting might be beneficial for at least some cases of resistance development to bevacizumab. The objectives of the current application are: 1) to study how VEGF interacts with this novel receptor in several different GBM cell lines, as well as in commercially available tissue arrays containing different grades of astrocytomas, and evaluate the physiological significance of such interaction, 2) To determine the interplay between this and other VEGF receptors/co-receptors, such as VEGFR-2, alpha v beta 3 integrin and nucleolin, and elucidate the cross-talk of their signalling pathways that subsequently activate the transcription factors NFAT and AP-1 and play a role in VEGF-induced cell migration, angiogenesis and inhibition of apoptosis. The project incorporates state of the art in vitro and in vivo approaches and is based on a multitude of disciplines, in order to validate an alternative target for GBM therapy, uncover novel or poorly explored signalling pathways, and identify potential bioactive molecules to be tested as inhibitors of GBM progression and angiogenesis.'

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