David vs. Goliath – how pathogens winds up the elaborate human DNA repair system

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Gastric cancer is one of the most common and often fatal cancers: Every third cancer death is due to gastric carcinoma. The main risk factor for the development of gastric cancer is chronic infection with an (almost) invisibly small pathogen – the stomach bacterium Helicobacter pylori.

Text and Photography by Martin Oeggerli

Since this bacterium was discovered in 1983, scientists have been struggling to explain the molecular mechanisms which triggers carcinogenesis. Now, research teams headed by Prof. Anne Mueller and Prof. Massimo Lopes from the Institute of Molecular Cancer Research at the University of Zurich have discovered how Helicobacter pylori harms human and animal host cells. The study has been published in the science journal PNAS.

The scientists report that the infection leads to DNA breaks in both strands of the double helix in infected cells. The frequency of double-strand breaks depends on the intensity and duration of the infection. Interestingly, infected cells are able to repair the majority of DNA breaks, if the bacterium is killed off with antibiotics within a few hours of infection. But prolonged infection exhausts the cell’s DNA repair system, leading to increased cell death and increased risk of mutations and stomach cancer. The new findings are an important step on the way to a better understanding and treatment of gastric cancer.


To throw light on the interaction between pathogen and host cells, ‘The Proceedings of the National Academy of Sciences (PNAS)’ has published a cover depicting human stomach cells which are heavily infected with Helicobacter pylori. The image was prepared and captured by Micronaut in collaboration with Anne Mueller and her team.

SEM scan: by Micronaut, kindly supported by School of Applied Sciences, FHNW, Muttenz.

Continue reading Atlant’s Column: Understanding Muscular Disease, August 2011, or go back to the archive