Helicobacter pylori (H. pylori)-infection leads to gastric cancer in human and rodents. The key determinants of this outcome are the severity and distribution of the H. pylori-induced inflammation. Bacteria or their products trigger this inflammatory process and the main mediators are cytokines. Identification of both host- and bacterial-factors that mediate is an intense area of interest in current researches. It has been demonstrated that oxidative and nitrosative stress associated with inflammation plays an important role in gastric carcinogenesis as a mediator of carcinogenic compound formation, DNA damage, and cell proliferation. Genetic information regulating such stress would be one of the host factors determining the outcome—particularly when the outcome is gastric cancer—of H. pylori infection, and the compound that attenuates such stress may be a candidate for use in chemoprevention. This review highlights recent advances in understanding of the mechanisms underlying gastric carcinogenesis following infection with H. pylori.
2005 by The Editorial Secretariat of JCBN