TMAC
TARGETING TUMOUR ASSOCIATED MACROPHAGES IN CANCER
| Coordinatore | INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM)
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
| # | ||||
|---|---|---|---|---|
| 1 |
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM)
Organization address
address: 101 Rue de Tolbiac contact info |
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 contact info |
FR (PARIS) | hostInstitution | 1˙499˙222.00 |
Mappa
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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.'