Stomach ulcers are caused by chronic infection with the Helicobacter pylori bacterium, which is also the leading risk factor for stomach cancer. One reason for the cancer risk could be that the pathogen creates breaks in the DNA molecules of infected cells, according to teams led by Massimo Lopes and Anne Müller at the University of Zurich in Switzerland.

The authors incubated mouse and human cells with the bacteria and found that the cells' DNA fragmented in a manner consistent with double-strand breakage. The breakage was dependent on direct contact between the cells and the bacteria, and was repaired by normal cellular machinery once the infection was over. However, when infection lasted for 48 hours or more, 70% of the cells stopped dividing, suggesting that continuous infection might overwhelm the DNA-repair mechanism.

Proc. Natl Acad. Sci. USA 108, 14944–14949 (2011)