Breast and ovarian cancers share many features, including genetic predisposition caused by mutations in BRCA1/2. Epithelial ovarian cancer is heterogeneous and associated with poor survival relative to breast cancer. Utilizing comprehensive biobanks, genomics methods and in vitro model systems we aim to improve our understanding of tumour evolution, heterogeneity and therapy response. Events underlying malignant transformation are poorly characterised in ovarian cancer, but accumulating evidence suggests that a majority of ovarian cancers arise in the Fallopian tube epithelium.

We aim to increase our understanding of the origin and early genomic events leading to the development of epithelial ovarian cancer. The heterogeneity of the disease requires improved knowledge of key processes involved in tumour initiation, development and maintenance for translation into truly personalised treatment. Identification of novel therapeutic targets, stratified by histological as well as mutational and transcriptional phenotypes, should transform survival prospects. Our goal is to elucidate the molecular context and mechanisms by which aberrantly regulated genes contribute to breast and ovarian tumorigenesis.

Improved knowledge ofthe molecular landscapes of these heterogeneous malignancies in the primary as well as metastatic setting may lead to the development of next generation biomarkers and biologically informed treatment strategies.