Liver Cancer breakthrough

International research involving the University of Adelaide has helped to better understand how a diseased liver promotes the development of cancer.

This work could lead to improvements in treating liver cancer, which is the second leading cause of cancer deaths worldwide.

For the first time, researchers have discovered that chronic inflammation of the liver suppresses the natural immune defence systems against cancer. This immune suppression enables the growth and potential spread of cancer.

In a further breakthrough, the research team has successfully used drugs and genetic engineering to switch off the inflammation-associated immune suppression, showing that the growth of cancer can be reversed or prevented.

“For many years, we’ve thought that inflammation directly affects liver cancer cells, stimulating their division and protecting them from cell death, helping them to grow and spread. However, we’ve now found that inflammation in a diseased liver actively prevents what we call ‘immunosurveillance’, the adaptive immune response which is part of the body’s frontline defence system against cancer,” co-author and leading international liver disease expert Professor Alastair Burt, Executive Dean of the Faculty of Health and Medical Sciences, University of Adelaide said.

Liver cancer is caused by chronic liver inflammation from hepatitis B or C, excess alcohol consumption, and diseases such as non-alcoholic steatohepatitis (NASH). Currently, the mainstay of treatment is surgical removal or ablation (the destruction of tumours).

“We’ve been able to switch off the active mechanism that interferes with the normal immune response. This has been done through the use of drugs, or by genetic engineering in mice, targeting a molecule known as PD-L1.

“When PD-L1 is inhibited, the normal adaptive immunity is no longer affected and can resume its job, suppressing and clearing tumours from the liver.”

The group’s research helps to explain why a class of drugs known as anti-PD-1 drugs, which block the receptor for PD-L1, may be effective at combating liver cancer.