Award for cancer immunology science

Research proving that the immune system roams the body hunting out malignancies has led to an international award for a Melbourne scientist.

The head of the Peter MacCallum Cancer Institute's cancer immunology program, Assoc Prof Mark Smyth, said the research was the first proof of a theory that forms the basis of cancer vaccine development worldwide.

The work, done in collaboration with US Professors Lewis Lanier and David Raulet, earned Smyth a prestigious William B Coley Award from the Cancer Research Institute of New York.

The award is granted to scientists with a distinguished body of research in basic and tumour immunology, with Smyth's research centred on understanding how the body's immune system responds to malignancy and metastasis of cancer.

His research was recognised for its groundbreaking findings on the critical role of natural killer cells of the immune system in eliminating spontaneously transformed cells.

"This award is related to very basic research into understanding the fact that cytotoxic lymphocytes, primarily T-cells, can roam around and identify degradation of cells before it becomes a malignancy," Smyth said.

T-cells have the ability to spontaneously kill virus-infected cells and cancer cells through an arsenal of molecules.

Smyth's research, using a knockout mouse bred without the protein perforin, involved determining how the components worked when cancer cells were killed.

His research group pinpointed perforin and interferon-gamma as being the major T-cell molecules used to wipe out tumours.

Perforin is a protein found housed in organelles inside the killer cells, which release granules when two cells come together and one is recognised as not being normal.

When killer cells recognise the tumour cell, they release the granules on the interface between the cells and perforin is secreted.

The perforin binds with other molecules to allow more killer cell granules to enter the foreign cell and trigger cell death.

The group examined spontaneous tumour development among perforin knockout mice compared to normal laboratory rodents, which have a much lower cancer incidence than humans because of their sterile environment.

Smyth said the work had shown that perforin protects against the development of mostly lymphomas, with the knockout mice showing a much greater prevalence of the cancer to the normal mice.

He said there had been some suggestion perforin might protect against lung adenocarcinomas.

The group now planned to concentrate their research on epithelial tumours, to see if the same principle applied.