Stomach cancer is the fourth most common form of cancer death in Australia and the second most common in parts of South Asia including Japan and Korea. Until now, little was known about what caused this disease, which is difficult to treat and usually incurable.
The team's discovery, a collaborative effort largely between the University of Melbourne and the Ludwig Institute for Cancer Research in Melbourne, has identified the possible targets for the development of drugs to treat these diseases. The research will be published in the October edition of the journal, Nature Medicine.
Using mice, Dr Matthias Ernst at the Ludwig and Associate Professor Andy Giraud from the University of Melbourne (Western Hospital) found the clue when they made specific mutations to a molecule found on the surface of cells that is traditionally involved in helping regulate the body's immune system.
The receptor molecule called, gp130, acts as a molecular 'antenna', to transmit instructions to individual cells from soluble messenger molecules called cytokines found in the circulation and body fluids. This message service is what tells the cell how to respond to its environment.
Ernst and Giraud were surprised when the mice carrying mutations in gp130 developed cellular changes and other symptoms that mirrored those of gastric cancer and large bowel inflammation in humans.
Previous research in the USA and Japan has largely dismissed the regulatory role that gp130 plays in the protection of the digestive tract against stomach cancer and some forms of inflammatory bowel disease.
"Nobody suspected that interference with the messenger service engaged by gp130 could be linked with a 100 percent prevalence of early stages of gastric cancer in mice," says Giraud.