Loss of cytostatic regulation by TGF-beta during EGFR-driven tumor development

Funding Activity

Website
http://purl.org/au-research/grants/nhmrc/433618

Funding Status
Closed

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Funded Activity Summary

Growth factor and cytokine signalling networks control many aspects of cell behaviour such as proliferation, survival, migration, invasive capabilities, transformation and differentiation. In normal cells, these complex signalling pathways are tightly regulated. Alterations of these signals are often found to cause, directly or indirectly, tumour formation. Transforming Growth Factor-b (TGF-b) and Epidermal Growth Factor (EGF) signalling pathways are both independently implicated as key regulators in tumour formation and as such they are potential therapeutic targets. However, while both pathways have been studied extensively, little is known about the cross-talk between the TGF-b and EGF pathways. This project will establish the generality of a new tumor signaling axis, namely EGFR-Stat3-Smad7-TGF-b in EGFR-overexpressing tumors. Practically, it will provide guidelines for the development of new approaches for treating effectively the EGFR-driven tumors.

Funded Activity Details

Start Date: 01-01-2007

End Date: 01-01-2010

Funding Scheme: Project Grants

Funding Amount: $605,031.00

Funder: National Health and Medical Research Council

Research Topics

ANZSRC Field of Research (FoR)

Oncology and Carcinogenesis

ANZSRC Socio-Economic Objective (SEO)

There are no SEO codes available for this funding activity

Other Keywords

Carcinogenesis | EGFR signaling | Smad | Stat | TGF-beta signaling | cell biology | signal transduction

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