BMDCMET

Innate and adaptive immune cell contribution to the pre-metastatic niche

Coordinatore	STICHTING HET NEDERLANDS KANKER INSTITUUT    more  Organization address address: PLESMANLAAN 121 city: AMSTERDAM postcode: 1066 CX contact info Titolo: Dr. Nome: Henri Cognome: Van Luenen Email: send email Telefono: 31205127979
Nazionalità Coordinatore	Netherlands [NL]
Totale costo	184˙040 €
EC contributo	184˙040 €
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-IEF
Funding Scheme	MC-IEF
Anno di inizio	2011
Periodo (anno-mese-giorno)	2011-06-01   -   2013-05-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	STICHTING HET NEDERLANDS KANKER INSTITUUT  Organization address address: PLESMANLAAN 121 city: AMSTERDAM postcode: 1066 CX contact info Titolo: Dr. Nome: Henri Cognome: Van Luenen Email: send email Telefono: 31205127979	NL (AMSTERDAM)	coordinator	184˙040.80

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 Obiettivo del progetto (Objective)

'Breast cancer metastasis is a foreboding and prevalent disease for women around the world. Over 90% of breast cancer deaths are caused by metastatic disease emphasizing the urgency for more research in this area. While experimental evidence indicates that tumor cells must acquire specific genetic mutations to disseminate and colonize distant organs, these genetic alterations are not sufficient for successful metastasis formation. The microenvironment of metastatic organs must also be pre-conditioned and adapted prior to the arrival of tumor cells. In other words, metastasis is not a passive event – a ‘pre-metastatic niche’ must be established. Bone marrow-derived cells (BMDCs) play a critical role in this process by secreting soluble factors to direct the recruitment of disseminated tumor cells to specific sites. Experimental studies suggest that both innate and adaptive immune cells initiate the pre-metastatic niche, but involvement of particular BMDC populations is largely dependent on tumor type. Together, these data support the hypothesis that breast cancer metastasis is not a passive event, but is regulated by specific BMDC populations in target organs. The overall goal of this application is to examine the cellular and molecular changes that occur in pre-metastatic organs and determine which are crucial for metastasis formation using a novel breast cancer metastasis model developed by the Host laboratory. To assess this, I propose to 1) Perform an in depth kinetic characterization of disseminated tumor cell colonization of distant metastatic organs; and 2) Determine which BMDC population regulates the pre-metastatic niche and their functional significance to metastasis formation. Evaluating the specific role of BMDCs in the initiation of metastases will identify novel targets for breast cancer patients to prevent future metastatic development and/or combat established metastases.'