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Chronic infection with Helicobacter pylori is a significant risk factor for gastric cancer, although the molecular mechanisms underlying the carcinogenesis are unclear. Recent work has suggested that the pathogen could be damaging the host genome, and investigators in Europe now provide a possible explanation.
Initial experiments revealed that infection of cultured gastric adenocarcinoma cells with H. pylori led to a dose-dependent fragmentation of cellular DNA consistent with induction of double-strand breaks (DSBs). Similar damage was found with infection of murine gastric epithelial cells and human osteosarcoma cells. DSB induction required direct attachment of live H. pylori cells to the host cells and was not linked to any of the H. pyl…