Published online Nov 7, 2015. doi: 10.3748/wjg.v21.i41.11654
Peer-review started: May 22, 2015
First decision: June 23, 2015
Revised: July 16, 2015
Accepted: September 22, 2015
Article in press: September 22, 2015
Published online: November 7, 2015
Helicobacter pylori (H. pylori) plays a role in the pathogenesis of gastric cancer. The outcome of the infection depends on environmental factors and bacterial and host characteristics. Gastric carcinogenesis is a multistep process that is reversible in the early phase of mucosal damage, but the exact point of no return has not been identified. Therefore, two main therapeutic strategies could reduce gastric cancer incidence: (1) eradication of the already present infection; and (2) immunization (prior to or during the course of the infection). The success of a gastric cancer prevention strategy depends on timing because the prevention strategy must be introduced before the point of no return in gastric carcinogenesis. Although the exact point of no return has not been identified, infection should be eradicated before severe atrophy of the gastric mucosa develops. Eradication therapy rates remain suboptimal due to increasing H. pylori resistance to antibiotics and patient noncompliance. Vaccination against H. pylori would reduce the cost of eradication therapies and lower gastric cancer incidence. A vaccine against H. pylori is still a research challenge. An effective vaccine should have an adequate route of delivery, appropriate bacterial antigens and effective and safe adjuvants. Future research should focus on the development of rescue eradication therapy protocols until an efficacious vaccine against the bacterium becomes available.
Core tip: Two main therapeutic strategies could reduce the incidence of Helicobacter pylori (H. pylori)-related gastric cancer: eradication of the infection or vaccination. Success of a gastric cancer prevention strategy depends on the eradication of the infection or on vaccination before irreversible mucosal changes (severe atrophy, intestinal metaplasia or dysplasia) have occurred. Eradication therapy results are suboptimal due to increased antibiotic resistance in H. pylori and patient noncompliance. To improve the rates of eradication, rescue regimens have been developed. Concomitant and sequential protocols seem equally effective rescue strategies. An effective vaccine is not available at present, in spite of enormous effort by different researchers.