P38CANCER

Signal integration and rewiring during tumor development

Coordinatore	FUNDACIO INSTITUT DE RECERCA BIOMEDICA (IRB BARCELONA)    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Spain [ES]
Totale costo	2˙497˙800 €
EC contributo	2˙497˙800 €
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-2011-ADG_20110310
Funding Scheme	ERC-AG
Anno di inizio	2012
Periodo (anno-mese-giorno)	2012-07-01   -   2017-06-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	FUNDACIO INSTITUT DE RECERCA BIOMEDICA (IRB BARCELONA)  Organization address address: CARRER BALDIRI REIXAC 10-12 PARC SCIENTIFIC DE BARCELONA city: BARCELONA postcode: 8028 contact info Titolo: Dr. Nome: Manuel Angel Cognome: Rodriguez Nebreda Email: send email Telefono: 34934031379 Fax: 34934020595	ES (BARCELONA)	hostInstitution	2˙497˙800.00
2	FUNDACIO INSTITUT DE RECERCA BIOMEDICA (IRB BARCELONA)  Organization address address: CARRER BALDIRI REIXAC 10-12 PARC SCIENTIFIC DE BARCELONA city: BARCELONA postcode: 8028 contact info Titolo: Ms. Nome: Raquel Cognome: Furió Email: send email Telefono: +3493 403 37 65 Fax: +3493 403 71 14	ES (BARCELONA)	hostInstitution	2˙497˙800.00

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 Obiettivo del progetto (Objective)

'Cell fate decisions rely on signaling pathways that integrate external signals to coordinate specific intracellular programs. One of these pathways leads to the activation of p38α MAPK, which plays key roles in cell responses to many types of stresses as well as chemotherapeutic agents and oncogenes. Importantly, p38α acts in a cell context-specific and cell type-specific manner to integrate signals that affect cell proliferation, differentiation and survival. Evidence from mouse models and human cell lines indicates that p38α can negatively regulate tumor initiation at different levels. Intriguingly, recent results suggest that p38α activation may also sometimes have pro-tumorigenic functions. The molecular basis for the different functions of p38α are not well understood but it is likely that the network of substrates phosphorylated by p38α plays a major role. This project proposes to investigate molecular mechanisms of p38 MAPK signaling during tumorigenesis including the systematic identification of substrates and how they contribute to the different functions of this pathway. An important part of the studies will focus on the mechanisms underlying the rewiring of p38α signaling to serve pro-tumorigenic functions, including in-depth characterization of how p38α regulates the survival, proliferation and spreading of cancer cells, as well as its role in the interplay between cancer cells and stromal cells. We also plan to investigate the implication of p38α in tumor progression in vivo, using both xenografts and genetically modified mice that we have generated to either inactivate or hyperactivate the p38 MAPK pathway. These models will allow us to analyze the role of this signaling pathway in the regulation of tumor initiation, growth and spreading in different tissues. Taken together, this project will address important questions on cellular signaling and tumor development, which might be also useful for more rational anti-tumoral treatments.'