Researchers report they have figured out how the cancer-causing bacterium Helicobacter pylori attacks a cell's energy infrastructure, sparking a series of events in the cell that ultimately lead it to self-destruct. H. pylori are the only bacteria known to survive in the human stomach. Infection with H. pylori is associated with an increased risk of gastric cancer, the second-leading cause of cancer-related deaths worldwide. "More than half the world's population is currently infected with H. pylori," said University of Illinois microbiology professor Dr. Steven Blanke, who led the study. "And we've known for a long time that the host doesn't respond appropriately to clear the infection from the stomach, allowing the bacterium to persist as a risk factor for cancer." The new study, published in the September 20, 2011 issue of the Proceedings of the National Academy of Sciences, is the first to show how a bacterial toxin can disrupt a cell's mitochondria – its energy-generation and distribution system – to disable the cell and spur apoptosis (programmed cell death). "One of the hallmarks of long-term infection with H. pylori is an increase in apoptotic cells," Dr. Blanke said. "This may contribute to the development of cancer in several ways." Apoptosis can damage the epithelial cells that line the stomach, he said, "and chronic damage to any tissue is a risk factor for cancer." An increase in apoptotic cells may also spur the hyper-proliferation of stem cells in an attempt to repair the damaged tissue, increasing the chance of mutations that can lead to cancer. Previous studies had shown that VacA, a protein toxin produced by H. pylori, induces host cell death, Dr.
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