We have two major research themes:

Lipid metabolism and cancer

We study how cancer cells acquire, store, and oxidise fatty acids; how lipid metabolism drives therapy resistance; and how the metabolic state of the host, including obesity and dyslipidaemia, shapes tumour behaviour. Current projects address fatty acid oxidation capacity and its contribution to the TCA cycle in cancer, the role of cardiolipin remodelling and ferroptosis sensitivity, cholesterol metabolism in therapy-resistant prostate cancer, and the systemic metabolic environment of melanoma and breast cancer. We work primarily with breast, prostate, and melanoma cancer models and maintain close collaborations with clinical researchers to ensure our findings translate to patient-relevant questions.

Lipid metabolism and metabolic disease

Disorders of lipid metabolism, including non-alcoholic fatty liver disease, insulin resistance, and obesity, share underlying mechanisms with the metabolic reprogramming seen in cancer. The laboratory applies its expertise in lipid flux measurement and lipidomics to understand how lipid droplet dynamics, fatty acid partitioning, and lipid species diversity contribute to metabolic dysfunction in liver and skeletal muscle, and how these processes interact with cancer biology in patients with co-morbid metabolic disease.

Cancers of the breast and prostate rank among the most common malignancies worldwide, and their incidence and severity are amplified by the global epidemic of obesity and metabolic disease. Existing treatments for these cancers are increasingly effective, but therapy resistance remains a major clinical challenge — and patients with poor metabolic health respond less well and relapse more frequently.

Our research aims to change this in three ways. First, by identifying the specific lipid metabolic pathways that cancer cells depend on, we create a rational basis for new targeted therapies that are less toxic and more durable than current approaches. Second, by characterising how obesity and dyslipidaemia alter the tumour environment, we are generating the molecular evidence needed to stratify patients, thereby ensuring that the right patients receive the right treatment. Third, by developing circulating lipid biomarkers in collaboration with clinical partners, we are translating our laboratory findings into tools that can inform treatment decisions.

Ultimately, we want to reduce the burden that cancer and metabolic disease together impose on patients, their families, and the health system.

Our work focuses on several areas:

• fatty acid oxidation in cancer — investigating why cancer cells maintain high fatty acid oxidation capacity, how this relates to TCA cycle fuelling and anaplerosis, and whether these features predict therapy sensitivity
• ferroptosis and lipid routing — characterising how the routing of fatty acids into specific lipid pools (including cardiolipin) determines ferroptosis susceptibility across cancer types
• cholesterol metabolism and therapy resistance — examining how LDL-cholesterol uptake, cholesteryl ester storage, and late endosomal cholesterol trafficking contribute to prostate cancer progression and resistance to androgen deprivation therapy
• tumour macroenvironment — understanding how the systemic metabolic environment, circulating lipids, adipokines, and immune cell metabolism, shapes tumour growth and immune evasion in breast cancer and melanoma
• lipid droplet biology in metabolic disease — dissecting the proteome and lipid composition of hepatic lipid droplets in insulin resistance and fatty liver disease.

• Associate Professor Andrew Hoy (Research group leader)