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Blocking the signal: Finding a way to stop cancer in its tracks

R&D Now

Pancreatic cancer currently offers sufferers little hope of survival, but a Curtin research team is making inroads by focusing on ways of blocking lipid signalling.

Pancreatic cancer is one of the most lethal diseases in Australia today. Although it is currently the eleventh most prevalent cancer diagnosed in the country, it is difficult to detect in the early stages, and once established, is highly aggressive and results in a high mortality rate. Resistant to both chemo and radiotherapy, a pancreatic cancer diagnosis presents the physician with few, if any, effective treatment options. Of around three thousand new cases of pancreatic cancer diagnoses nationally in 2015, only six per cent of sufferers will survive to five years following diagnosis.

There is an urgent need to understand more about how this disease is initiated and proliferates, in order to develop treatments and cures.

Professor Marco Falasca from Curtin’s School of Biomedical Sciences is heading a team committed to finding cures and treatments for patients with chronic diseases, in particular challenging illnesses, such as pancreatic cancer.

His current focus is on the role of metabolism in the pancreatic function, specifically intracellular signals regulated by specific lipids that act as ‘second messengers’ inside a cell to control a plethora of cellular functions, including cell growth, proliferation and metabolism.

Funded by European Union Research Funding, Diabetes UK, British Heart Foundation, Pancreatic Cancer Research Fund and Prostate Cancer UK, among others, Professor Falasca and his team have studied how lipid signalling acts in cancer. Their findings have included an understanding that from the initial stages of pancreatic cancer, lipid signalling is hyperactivated, and this in turn affects the proliferation of cells. Finding a means of blocking the hyperactivated signals could assist in halting or degrading the proliferation of cancerous cells, slowing or stopping the spread of the disease.

“We are paying particular attention to lipids known as phosphoinositides, such as Lysophosphatidylinositol (LPI), that can themselves act as, or be converted into, messengers, ultimately regulating several cellular functions. In recent years, our work on proteins involved in LPI mechanism of action, such as ABC transporters and G protein-coupled receptors, has revealed a novel mechanism for these proteins in cancer progression and cell signalling. LPI is a bioactive lipid that is able to activate signalling cascades relevant to cell proliferation, migration, survival and tumourigenesis,” Professor Falasca explains.
This enhanced understanding of the pivotal role that LPI signalling and its effect on G protein-coupled receptors plays in the progress of cancer, has advanced to the point where Professor Falasca and his team have been able to test various drug combinations aimed at breaking that nexus, and perhaps halting the proliferation of cancerous cells.
“We have recently discovered a very promising drug combination that is currently under evaluation for testing in clinical trials,” he says.

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