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Blocked Bacteria Protects Against Stomach Cancer

As antibiotic resistance has reduced the effectiveness of treatments for a bacterium associated with stomach cancer, researchers from the Murdoch Childrens Research Institute have found a way to switch on the production of a protein that prevents infection.

The bacterium Helicobacter pylori triggers inflammation of the stomach lining, causing peptic ulcers and stomach cancer. Current preventative therapy for stomach cancer is based on antibiotic eradication of H. pylori. However, an increased global prevalence of antibiotic-resistant H. pylori strains has reduced their effectiveness, leading to efforts to find new ways to combat stomach cancer.

Dr Treve Menheniott and Prof Andy Giraud found that Gastrokine-2 (GKN2), a protein normally present at high levels in the healthy human stomach, is switched off in people with stomach cancer, and suggest that it might function to protect against H. pylori infection.

The team found that GKN2-deficient mice that were infected with H. pylori developed more severe stomach inflammation and experienced accelerated pre-cancerous disease and tumours than mice with normal GKN2 levels. When normal levels of GKN2 were restored, tumour growth was significantly inhibited.

Menheniott says that the findings identify GKN2 as a critical suppressor of inflammation-driven stomach cancer. “GKN2 may have novel therapeutic value in 15% of infected individuals for whom antibiotic treatment fails or in people with irreversible pre-cancerous stomach lesions,” he says.

Giraud said that the research could help protect those at risk of stomach cancer by inhibiting tumour growth. “While the survival rate for people with stomach cancer is only around 27%, these findings are really exciting for us because stomach cancer can be treated much more efficiently if diagnosed early,” he said.

The research has been published in the Journal of Clinical Investigation (