The transformation of normal breast tissue to tumor requires the accumulation of mutations, which is readily achieved by deregulation of DNA repair pathways. We found that metastatic breast cancers have high levels of the DNA repair protein RAD51. Metastatic breast cancer represents a subtype that has poor clinical outcome and is often resistant to conventional chemotherapies. We have created breast cancer cell lines that mimic chemotherapy resistant tumours. We want to examine these cells to determine the mechanisms that support chemoresistance; with a focus on the DNA repair pathways. Outcomes from these analyses will provide new potential clinical targets in treating metastatic breast cancer.
- Project 1: Defining markers of genome stability that contribute to chemoresistance.
- Project 2: Defining DNA repair pathways in circulating tumour cells that support metastasis.
- Suitable for Honours or PhD students.