Within an individual, the development of cancer results from a combination of factors, including circumstances of infection, the individual's genetic makeup, H. pylori strain type, and other cofactors. Only some of these risk factors are amenable to intervention within a population. H. pylori-related gastric cancer could be prevented by preventing H. pylori infection (through either the interruption of H. pylori transmission or the immunization of susceptible people); by curing H. pylori infection (with the treatment of infected people via antibiotic therapy or therapeutic vaccination); or by removing other factors necessary for gastric cancer development.
H. pylori is decreasing in prevalence with time. Estimates of the decline over the century range from 26% to 52% per decade (41,42,176,177). It is not known why the organism is disappearing, but improvements in nutrition, household sanitation, and household crowding are likely factors. Thus as countries improve their socioeconomic conditions, infection rates should continue to decline around the world. At the current rate, H. pylori could disappear from some populations entirely within the next few generations (M. Rupnow, personal communication).
Meanwhile, prophylactic vaccines could prevent infection with H. pylori in unin-fected at-risk persons, primarily children and young adults. Although several oral and intranasal vaccines have been shown to provide protective mucosal immunity against H. pylori in both mice and monkeys (179-183), many years will be required until a vaccine shown to be successful in animal models is proven safe and efficacious in humans (184,185). Because some of the damage caused by H. pylori may result from an autoimmune response, vaccination actually might induce a chronic inflammatory response (181).
H. pylori infection can be eradicated by antibiotic therapy. To date, screening for and treatment of H. pylori are recommended only for persons in specific high-risk groups (186,187). A key reason for this selection is that it is not known whether eradication of infection prevents gastric cancer. If antibiotic therapies could prevent a small percentage of cancers (e.g., 20-30%), screening and treatment of H. pylori would be a cost-effective strategy to preventing cancer (188,189). Current trials in Europe and China (190) are examining the preventive ability of H. pylori eradication and have randomized thousands of infected people to H. pylori therapy or placebo with follow-up for gastric cancer incidence over 10-20 yr. If treatment is shown to be effective in reducing cancer rates, these studies will prove that H. pylori causes malignancy and that screening and treatment are warranted. Unfortunately, studies of this type are extremely expensive in both logistics and follow-up time; they also run the risk of insufficient statistical power due to decreasing cancer rates and H. pylori prevalence.
An alternative and cheaper study design examines intermediate biomarkers instead of cancer. Subjects with gastric preneoplastic conditions are randomized to receive either H. pylori therapy or placebo and monitored for the progression or regression of these conditions. These studies, also ongoing, will not be able to prove that treatment of H. pylori will prevent cancer, as even if preneoplastic conditions regress, cancer could still occur. To date, small case series that have looked at regression of preneo-plastic conditions have yielded mixed results (191-195), although one has suggested that H. pylori eradication not only can prevent cancer, but it can also do so at a very late stage in tumor development (195).
It is important to recognize that H. pylori infection might actually have a beneficial effect. For example, recent studies suggest that H. pylori infection protects against the development of reflux esophagitis, and adenocarcinoma of the gastric cardia and gastroesophageal junction (196,197). Thus, trials of H. pylori eradication should assess all-cause mortality, not just mortality from noncardia gastric cancer.
Alternative targets for gastric cancer prevention involve environmental cofactors. As mentioned previously, dietary supplementation with antioxidants, or diets rich in fresh fruit have been associated with a decreased gastric cancer risk and are beneficial for many reasons (198,199). Cigarette smoking has also been linked to gastric tumors, among many other conditions (171).
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