CAF AND INFLAMMATION

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

 Coordinatore 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

 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

Mappa


 Word cloud

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

inflammation    tumors    inflammatory    primary    mortality    metastatic    breast    tumor    tumorigenesis    mammary    cafs    signaling    metastasis    related    stroma    fibroblasts    cancer   

 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.'

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