Targeting Tumour Dormancy in Breast Cancer
Finish Year: 2008
Chief Investigator: Associate Professor Erik Thompson
Tumour cells from primary cancers in the breast are able to spread around the body, lodge in different tissues and lie dormant for up to 20 years. For reasons we do not understand, the tumour cells are triggered to start growing, resulting in formation of secondary tumours that tend to be resistant to our normal therapies. This is one of the major obstacles to complete cure of breast cancer and carries with it, a large emotional burden for patients.
Research in recent years has shown that a process called epithelial to mesenchymal transition (EMT) occurs in normal cells during development and can be hijacked by cancer cells to provide them with a means of spreading around the body. Associate Professor Thompson hypothesises that EMT contributes to tumour cell dormancy by holding cells in a state that allows them to resist stresses such as a lack of sufficient oxygen (hypoxia), chemotherapy or radiotherapy.
The aim of this national program is to: use new genomic technologies and mouse models of breast cancer to identify novel molecules and pathways that regulate EMT and/or regulate tumour dormancy; confirm that these molecules and pathways are found in human breast cancer samples; study how these molecules and pathways contribute to EMT and tumour cell dormancy; determine whether inflammatory stresses and injury are responsible for the growth of secondary tumours from dormant cells; examine EMT indices in clinical material collected before treatment and after relapse, and from metastatic sites; and to enter the most promising candidates into a national collaborative program seeking new therapies for cancer (CRC-CT). Drug candidates will be optimised for preclinical and clinical testing.
Knowledge of these molecules and processes will certainly allow us to design and develop treatment therapies over and above our current armamentarium.