A drug for the prevention of Cancer also disables H. pylori bacterium

Researchers from Vanderbilt have discovered that a medicine that is presently being examined as an agent of chemoprevention for several kinds of cancer has more potential than stomach cancer prevention.

Researchers have concluded that in addition to blocking the cell growth production compounds, DMFO (difluoromethylornithine) drug directly acts on the Helicobacter pylori bacterium in order to lower its virulence. The H. pylori infection is also the basic cause of gastric cancer.

Half of the human population’s stomach is affected by H. pylori however only 1% of the infected people become a patient of stomach cancer. The stomach cancer can be prevented by treating the infection but it is still not clear who can be treated.

“H. pylori has co-evolved with humans for at least 60,000 years, probably longer, and attempting to prevent stomach cancer by eliminating the infection with widespread use of antibiotics is not necessarily a good idea,” said Senior Professor of Medicine, Keith Wilson.

“Our study suggests that it might be possible to reduce the virulence of the bacteria, without having to eliminate it. It’s a speculative and unusual way to think about an infection, but it could be an interesting strategy.”

Director of ‘Vanderbilt Center of Mucosal Inflammation and Cancer’, Wilson and his team recently associated the development of compounds for cell growth called polyamines to the stomach cancer development in an animal model that was H. pylori-infected. They showed that the treatment of animals with DMFO that inhibits an enzyme is basically a key for the polyamines production that prevents stomach cancer.

“What we noticed is that bacterial strains coming from DFMO-treated animals have reduced ability to move this virulence factor into epithelial cells,” Sierra explained.

“This drug (DFMO), which inhibits a very specific enzymatic pathway, also has what some might call ‘off target’ effects: it causes mutations in an H. pylori gene that affects the translocation of CagA,” explained Wilson. “The vast majority of gastric cancer is associated with strains that are CagA-positive. If this drug interferes with CagA activity, that’s an added bonus.”