What we do

Our focus is on understanding how tumour suppressors may be involved in the development of cancer, in particular genes that regulate Receptor Tyrosine Kinases (RTKs). One such gene is OPCML, which is present in normal cells but is subsequently switched off in cancer, resulting in poor survival outcomes. We are interested in understanding how this gene is regulated, how it functions in cells, and how it could ultimately be used as a therapeutic. 

Why it is important

RTKs are often overactive in several cancer types. They act like the accelerator pedal in a car; tumours therefore grow uncontrollably, spread around the body and become resistant to therapy. Drugs that block specific RTKs have shown to be beneficial in many cancers; however, cancer cells are complex and are capable of bypassing these drugs - our OPCML based drug strategy seeks to both stop RTK activation, and solve this complex bypass problem.

How it can benefit patients

By targeting genes that regulate RTKs, there is potential to develop novel gene-based cancer therapies to benefit patients. Due to the location and site of action of OPCML on the cell surface, there is a rare opportunity to reintroduce this tumour suppressor function back into the cancer cells in the form of a OPCML based drug. Furthermore, since OPCML is a normal product of healthy cells, its use as therapeutic should result in minimal toxicity.

Summary of current research

• Understanding the mechanism of OPCML trafficking in cells, i.e. how it moves in and out cells
• Understanding how OPCML associates with its interacting partners (e.g. RTKs) and how it modulates their function
• Structural biology of OPCML
• Therapeutic development of OPCML as an anti-cancer drug
• Development of new model systems

Our researchers