<P> Two related mechanisms by which H. pylori could promote cancer are under investigation . One mechanism involves the enhanced production of free radicals near H. pylori and an increased rate of host cell mutation . The other proposed mechanism has been called a "perigenetic pathway", and involves enhancement of the transformed host cell phenotype by means of alterations in cell proteins, such as adhesion proteins . H. pylori has been proposed to induce inflammation and locally high levels of TNF - α and / or interleukin 6 (IL - 6). According to the proposed perigenetic mechanism, inflammation - associated signaling molecules, such as TNF - α, can alter gastric epithelial cell adhesion and lead to the dispersion and migration of mutated epithelial cells without the need for additional mutations in tumor suppressor genes, such as genes that code for cell adhesion proteins . </P> <P> The strain of H. pylori a person is exposed to may influence the risk of developing gastric cancer . Strains of H. pylori that produce high levels of two proteins, vacuolating toxin A (VacA) and the cytotoxin - associated gene A (CagA), appear to cause greater tissue damage than those that produce lower levels or that lack those genes completely . These proteins are directly toxic to cells lining the stomach and signal strongly to the immune system that an invasion is under way . As a result of the bacterial presence, neutrophils and macrophages set up residence in the tissue to fight the bacteria assault . </P> <P> The pathogenesis of H. pylori depends on its ability to survive in the harsh gastric environment characterized by acidity, peristalsis, and attack by phagocytes accompanied by release of reactive oxygen species . In particular, H. pylori elicits an oxidative stress response during host colonization . This oxidative stress response induces potentially lethal and mutagenic oxidative DNA adducts in the H. pylori genome . </P> <P> Vulnerability to oxidative stress and oxidative DNA damage occurs commonly in many studied bacterial pathogens, including Neisseria gonorrhoeae, Hemophilus influenzae, Streptococcus pneumoniae, S. mutans, and H. pylori . For each of these pathogens, surviving the DNA damage induced by oxidative stress appears supported by transformation - mediated recombinational repair . Thus, transformation and recombinational repair appear to contribute to successful infection . </P>

Infection with the bacterium helicobacter pylori (h. pylori)