DNA damaging agents (radiation and chemotherapeutic drugs) play a major role in the treatment of cancer. In tumours displaying high treatment sensitivity, these agents activate apoptotic pathways while resistant tumours show a blockade of these pathways. This project focuses on the analysis of the interplay between mitochondria and the p53 family proteins, sensors of DNA damage, in order to identify and verify new molecular targets responsible for therapy resistance of tumour cells. The main long-term goal of this proposal is to elucidate the mechanisms accounting for tumour resistance to killing, in order to allow the development of new strategies for cancer therapy. Research groups involved in this proposal have long track records in apoptosis research and are now joining efforts with a clinical partner engaged in exploring apoptotic mechanisms of treatment resistance in lung cancer. In addition, an industrial partner will join the project to provide genomic and bioinorganic capabilities and a route to commercial exploitation.
Funding SchemeCSC - Cost-sharing contracts