Unravelling the cellular and spatial heterogeneity in prostate cancer to identify drivers of disease progression and treatment resistance

The growth of prostate cancer requires hormones called androgens, therefore current therapies for advanced prostate cancer generally work to block androgen production or action. Unfortunately, most patients develop resistance to these therapies, and this treatment-resistant stage of disease has no cure. We now appreciate that prostate tumours contain a diverse mixture of cells that form the tumour microenvironment and constantly interact with each other to influence tumour growth, progression, and response to treatment.

Our team are world-renowned for our patient-derived tumour model, wherein pieces of tumour from men undergoing surgery for prostate cancer are cultured in the laboratory in a way that uniquely retains the native structure and cell-to-cell interactions of the tumour microenvironment. Coupling this model with advanced sequencing technology and computational data analysis will enable us, for the first time, to profile individual tumours from patients to study features of the tumour microenvironment prior to treatment and to determine how these features change upon treatment. This information will help us identify specific cell populations and interactions that are responsible for poor patient outcomes and how they fuel tumour growth and survival after treatment.

If successful, my fellowship will establish new approaches to identify patients at high risk of disease progression or treatment failure, and explain how these tumours evade treatment to develop better treatment strategies that will more effectively kill cancer cells to prevent treatment resistance.