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Challenges to successful treatment of oesophageal cancer are the presence of viable drug resistant cells following chemotherapy. This enables the cancer to re-emerge at a later time point which is frequently more aggressive. Autophagy is a cell process activated in times of stress. We have shown that oesophageal cancer cells that induce autophagy show a remarkable ability to recover when chemotherapy drugs have been removed. In contrast cells that induce another form of cell death - apoptosis are unable to recover following drug treatment. However, pushing autophagy to excess can also result in the death of cells. Through our research, we have identified novel prospective regulators of these processes. The aim of this project is to investigate the potential involvement of these targets in determining the response of cancer cells to chemotherapeutics. Ultimately, we wish to alter these regulators to prevent the resistance mechanism and promote cell death. These results may improve current treatment regimes and eliminate disease recurrence in cancer patients.
Oesophageal cancer is a highly aggressive disease which often develops resistance to chemotherapy following initial treatment. Through activation of a cell stress process called autophagy, oesophageal cancer cells are capable of recovering from initial chemotherapy treatment. However, if cancer cells induce excessive autophagy, then the therapeutic outcome is much improved. This project aims to identify novel regulators of this stress process which may improve treatment outcomes and reduce the incidence of disease recurrence.
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