Many epidemiological reports indicate that Helicobacter pylori (H pylori)
infection plays an important role in gastric
carcinogenesis. Several genetic and epigenetic alterations contribute to the initiation, promotion, and progression of the
cancer cells in a multi-step manner. H pylori is known to induce chronic
inflammation in the gastric mucosa. Its products, including
superoxides, participate in the DNA damage followed by initiation, and the
inflammation-derived
cytokines and
growth factors contribute to the promotion of gastric
carcinogenesis. By eradicating H pylori, gastric
inflammation can be cured; the
therapy diminishes the levels not only of inflammatory cell infiltration, but also
atrophy/intestinal
metaplasia in part. A randomized controlled trial revealed that the eradication
therapy diminished the
gastric cancer prevalence in cases without pre-cancerous conditions. In addition, recent epidemiological studies from Japanese groups demonstrated that the development of
gastric cancer, especially of the intestinal type, was decreased by successful eradication
therapy, although these were designed in a non-randomized manner. However, it should be mentioned that endoscopic detection is the only way to evaluate the degree of gastric
carcinogenesis. We have reported that the endoscopic and histological morphologies could be modified by eradication
therapy and it might contribute to the prevalence of
gastric cancer development. Considering the biological nature of
cancer cell proliferation, it is considered that a sufficiently long-term follow-up would be essential to discuss the anticancer effect of eradication
therapy.