CAF AND INFLAMMATION

Defining the molecular mechanisms of fibroblast-mediated inflammation and its role in cancer progression and metastasis

Coordinatore	TEL AVIV UNIVERSITY    more  Organization address address: RAMAT AVIV city: TEL AVIV postcode: 69978 contact info Titolo: Ms. Nome: Lea Cognome: Pais Email: send email Telefono: 97236408774 Fax: 97236409697
Nazionalità Coordinatore	Israel [IL]
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-2010-RG
Funding Scheme	MC-IRG
Anno di inizio	2011
Periodo (anno-mese-giorno)	2011-03-01   -   2015-02-28

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	TEL AVIV UNIVERSITY  Organization address address: RAMAT AVIV city: TEL AVIV postcode: 69978 contact info Titolo: Ms. Nome: Lea Cognome: Pais Email: send email Telefono: 97236408774 Fax: 97236409697	IL (TEL AVIV)	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'Breast cancer is one of the leading causes of cancer related mortality in women in the western world and inflammation is correlated with bad prognosis in breast cancer. Breast tumors are characterized by an extensive desmoplastic stroma, abundantly populated by fibroblasts. Cancer Associated Fibroblasts (CAFs) have been shown to promote the growth of mammary tumors by directly stimulating tumor cell proliferation and by enhancing angiogenesis, but their role in mediating inflammation in breast tumorigenesis is unknown. Despite the fact that most of cancer-related mortality is a result of tumor metastasis, and not of the primary tumor, very little is known to date about the role of the metastatic stroma in allowing disseminated tumor cells from the primary tumor to propagate and colonize the metastatic organ. Even less is known about the role of fibroblasts in this critical stage of the metastatic cascade. Using a genetically engineered mouse model of mammary carcinoma we will investigate pro-inflammatory signaling by CAFs during different stages of mammary tumorigenesis, starting at early hyperplastic lesions, elucidate its functional importance and define the molecular pathways that underlie inflammatory signaling by mammary CAFs in tumor progression and metastasis.'