Prostate cancer is a high-incidence male cancer which progresses to lethal metastatic disease in around 20-30% of diagnosed cases.
Our research focus is on identifying biological drivers of disease progression. In so doing we have used genetic, genomic and transcriptomic approaches to show that prostate cancer cells undergo metabolic dysregulation in the early stages of the disease with concomitant stress resistance linked to the unfolded protein response and nucleolar biogenesis.
Our entry-points have been the study of transcription factors, the androgen receptor and c-Myc in particular. We are now endeavouring to generate pre-clincial models which better define the reprogramming factors that best reflect the transition for localized to metastatic disease.