TMAC

TARGETING TUMOUR ASSOCIATED MACROPHAGES IN CANCER

Coordinatore	INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM)    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	France [FR]
Totale costo	1˙499˙222 €
EC contributo	1˙499˙222 €
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-2010-StG_20091118
Funding Scheme	ERC-SG
Anno di inizio	2010
Periodo (anno-mese-giorno)	2010-12-01   -   2015-11-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM)  Organization address address: 101 Rue de Tolbiac city: PARIS postcode: 75654 contact info Titolo: Dr. Nome: Toby Cognome: Lawrence Email: send email Telefono: 33491269166 Fax: 33491269430	FR (PARIS)	hostInstitution	1˙499˙222.00
2	INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM)  Organization address address: 101 Rue de Tolbiac city: PARIS postcode: 75654 contact info Titolo: Ms. Nome: Veronique Cognome: Legros Email: send email Telefono: +33 491 827 015 Fax: +33 491 742 067	FR (PARIS)	hostInstitution	1˙499˙222.00

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 Obiettivo del progetto (Objective)

'There is increasing evidence that the body s ability to mount an immune response to cancer cells may dictate which patients are cured of cancer by conventional therapy. Macrophages have a central role in both innate and adaptive immunity; both human and experimental cancers become infiltrated by macrophages, however tumour-associated macrophages (TAM) are corrupted by the tumour microenvironment to promote survival, invasion and metastasis of cancer cells. TAM also contribute to immune-suppression in cancer and evasion of anti-tumour immunity. It is not clear what factors promote the pro-tumour TAM phenotype or the signalling pathways involved. The intrinsic anti-tumour potential of macrophages as innate immune cells and their abundance in solid tumours makes them an attractive therapeutic target. The challenge is to block the cancer-promoting function of these cells and restore their anti-tumour effects. We have previously shown that NF-ºB inhibits the classical activation of macrophages in the context of inflammation and cancer and our preliminary data show that NF-ºB activation in TAM inhibits anti-tumour immunity in transplantable models of cancer. Further studies have shown a subset of IKK²-regulated genes in macrophages are dependent on p38 MAP Kinase (MAPK14) and targeting p38 activity in macrophages also blocks the TAM phenotype. These data suggest IKK²-p38 signalling maintains the pro-tumour phenotype of TAM and inhibits anti-tumour immunity.In this project we will extend our preliminary observations in transplantable tumour models to clinically relevant genetic models of spontaneous cancer in mice. We will also map IKK² and p38 target genes in TAM and investigate IKK²/p38 dependent mechanisms of gene regulation.'