Triple Negative Breast Cancers (TNBC) represent the subtype of breast cancer with the poorest clinical outcomes. At present we do not know the molecular drivers of TNBC, therefore, these tumours do not have targeted therapies available and are treated with a generic cocktail of chemotherapy drugs. We are working to identify new biomarkers of response to current therapies so we can predict which patients will need additional or more intensive treatments. We are also trying to identify the genes/pathways driving TNBC growth and spread so that we can develop novel targeted therapies. This includes elucidation of the role of T-box2 (TBX2), a poor outcome marker present in TNBC and other breast cancer subtypes; and the role of the cGAS-STING immune pathway in response to cytoplasmic DNA, a by-product of DNA damage.

Our work also examines on the discovery and characterisation of inherited germline variation that influences risk of breast cancer. We use large scale genetic epidemiology studies to identify regions of the genome that are associated with susceptibility to female and male breast cancer, then perform laboratory investigation of these regions to identify gene targets that are regulated by genetic risk factors so that we may gain a better understanding of the biological processes that underpin cancer predisposition.

The most common and aggressive form of ovarian cancer is High Grade Serous Carcinomas (HGSCs). Five year survival rates for HGSCs have remained unchanged (35-40%) for the past three decades. There is no effective screening tool for HGSCs and they are usually detected in the later stages of the disease (FIGO stages 3/4), at which point they have already spread beyond the ovaries.

We have identified numerous DNA methylation events occurring early in the pathogenesis of HGSC and are currently developing new early detection approaches to identify these changed with the aim of improving survival outcomes.