Home > Stomach (Gastric) Cancer Prevention (PDQ®): Prevention - Health Professional Information [NCI]
This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER.
Note: Separate PDQ summaries on Stomach (Gastric) Cancer Screening, Gastric Cancer Treatment, and Levels of Evidence for Cancer Screening and Prevention Studies are also available.
Who Is at Risk?
People at elevated risk for gastric cancer include elderly patients with atrophic gastritis or pernicious anemia, patients with sporadic gastric adenomas, familial adenomatous polyposis, or hereditary nonpolyposis colon cancer, and immigrant ethnic populations from countries with high rates of gastric carcinoma.[4,5] Workers in the rubber and coal industries are also at increased risk.
Risk factors for gastric cancer include the presence of precursor conditions such as chronic atrophic gastritis and intestinal metaplasia, pernicious anemia, and gastric adenomatous polyps. Genetic factors include a family history of gastric cancer, Li Fraumeni syndrome, and type A blood type. Environmental factors include low consumption of fruits and vegetables; consumption of salted, smoked, or poorly preserved foods; cigarette smoking; and radiation exposure.[6,7,8]
There is consistent evidence that Helicobacter pylori infection, also known as H. pylori infection, of the stomach is strongly associated with both the initiation and promotion of carcinoma of the gastric body and antrum and of gastric lymphoma.[9,10,11] The International Agency for Research on Cancer classifies H. pylori infection as a cause of noncardia gastric carcinoma and gastric low-grade B-cell mucosa-associated lymphoid tissue or MALT lymphoma (i.e., a Group 1 human carcinogen).[12,13] Gastric cancer has been observed to be more common among individuals who use proton pump inhibitors (PPIs), relative to nonusers, after apparent successful H. Pylori eradication therapy, but confounding and detection bias cannot be ruled out as explanations.
Compared with the general population, people with duodenal ulcer disease may have a lower risk of gastric cancer.
Interventions for Reduction of Stomach (Gastric) Cancer Risk
Based on solid evidence, smoking is associated with an increased risk of stomach cancer.[16,17,18] The 2004 Surgeon General's report identifies cigarette smoking as a cause of stomach cancer, with an average relative risk (RR) in former smokers of 1.2 and in current smokers of 1.6. Compared with persistent smokers, the risk of stomach cancer decreases among former smokers with time since cessation. This pattern of observations makes it reasonable to infer that cigarette smoking prevention or cessation would result in a decreased risk of gastric cancer.
Magnitude of Effect: A systematic review and meta-analysis showed a 60% increase in gastric cancer in male smokers and a 20% increase in gastric cancer in female smokers compared with nonsmokers.
H. Pyloriinfection eradication
Based on solid evidence, H. pylori infection is associated with an increased risk of gastric cancer. A meta-analysis of seven randomized studies, all conducted in areas of high-risk gastric cancer and all but one conducted in Asia, suggests that treatment of H. pylori may reduce gastric cancer risk (from 1.7% to 1.1%; RR = 0.65; 95% confidence interval, 0.43–0.98). Only two studies assessed gastric cancer incidence as the primary study outcome, and two different studies were double blinded. It is unclear how generalizable the results may be to the North American population.
In the initial report from a clinical trial, 3,365 randomized subjects were followed in an intention-to-treat analysis; it was shown that short-term treatment with amoxicillin and omeprazole reduced the incidence of gastric cancer by 39% during a period of 15 years following randomization, with similar but not statistically significant reductions for gastric cancer mortality.
Magnitude of Effect: Risk of cancer may be reduced; effect on cancer mortality is not known.
Interventions With Inadequate Evidence as to Whether They Reduce the Risk of Stomach (Gastric) Cancer
Based on fair evidence, excessive salt intake and deficient dietary consumption of fresh fruits and vegetables are associated with an increased risk of gastric cancer. Dietary intake of vitamin C contained in vegetables, fruits, and other foods of plant origin is associated with a reduced risk of gastric cancer. Diets high in whole-grain cereals, carotenoids, allium compounds, and green tea are also associated with a reduced risk of this cancer. However, it is uncertain if changing one's diet to include more vegetables, fruits, and whole grains would reduce the risk of gastric cancer.
Magnitude of Effect: Small, difficult to determine.
Incidence and Mortality
The age-adjusted incidence rate for gastric cancer in the United States for the years 2004 to 2008 was 7.7 persons per 100,000 population. Incidence among men is twice as high as among women. Mortality rates for gastric cancer have been declining worldwide in recent decades, most prominently in the United States.[2,3] Mortality rates for white males in the United States were approximately 40 deaths per 100,000 population in 1930, compared with 4.6 deaths per 100,000 population for the years 2003 to 2007. The death rate from gastric cancer for black males was 2.3 times higher than for whites for the years 2003 to 2007. The annual number of new cases seems to be steady in recent years; in 2018, it is estimated that 26,240 Americans will be diagnosed with gastric cancer and 10,800 persons will die of it. Gastric cancer is the fourth most common cancer in the world.[6,7] Worldwide, the estimated number of cases per year in 2008 was 988,000, and the estimated number of deaths was 736,000. Age-standardized annual incidence rates vary widely across the world: from 3.9 to 42.4 cases per 100,000 in men, and from 2.2 to 18.3 cases per 100,000 in women. More than 70% of cases occur in developing countries, and 50% of the cases occur in Eastern Asia.
Most gastric cancers in the United States are advanced at diagnosis, which is reflected in an overall 5-year survival rate of 29.9% from 2005 to 2011. Carcinomas localized to the mucosa or submucosa ("early" cancers) have a much better prognosis; the 5-year survival rate is more than 95% in Japan and more than 65% in the United States. In high-risk populations, secondary prevention measures linked to screening programs have been instituted. In Japan, endoscopic resection techniques have been refined and could possibly be responsible for drastic reductions in mortality rates in the presence of steady incidence rates. This hypothesis, however, has not been tested in clinical trials. (Refer to the PDQ summary on Stomach (Gastric) Cancer Screening for more information.)
Understanding the pathogenesis of gastric cancer has advanced over the years. A lengthy precancerous process has been identified in which the gastric mucosa is slowly transformed from normal to chronic gastritis, to multifocal atrophy, to intestinal metaplasia of various degrees, to dysplasia, and then to invasive carcinoma. The process is apparently driven by forces acting on the gastric epithelium for many years, such as excessive dietary salt and most prominently, infection with Helicobacter pylori.
A systematic review and meta-analysis showed a 60% increase in gastric cancer in male smokers and a 20% increase in gastric cancer in female smokers compared with nonsmokers. A systematic review of studies addressing the relationship between cigarette smoking and gastric cancer to estimate the magnitude of the association for different levels of exposure to cancer provides solid evidence to classify smoking as the most important behavioral risk factor for gastric cancer.[11,12,13] Compared with persistent smokers, the risk of stomach cancer decreases among former smokers with time since cessation. The pattern that emerges from these observations makes it reasonable to infer that cigarette smoking prevention or cessation would result in a decreased risk of gastric cancer.
H. pyloriinfection eradication
H. pylori infection is an accepted cause of gastric adenocarcinoma.[14,15] Questions remain concerning the natural history of H. pylori infection; the mechanism of transmission and the rates of reinfection or recrudescence for different populations are unknown.[16,17] A small randomized trial of antibiotic eradication in 140 H. pylori-infected people suggests the possibility of transmission among close family members. In 70 participants, only the participant received eradication therapy; in the other 70 participants, all H. pylori-infected family members living with the primary participant also received the eradication therapy. Nine months after the therapy, the positivity rates in the index participants in each group were 38.6% and 7.1%, respectively (odds ratio = 8.61; 95% confidence interval [CI], 2.91–22.84), suggesting the possibility of transmission from untreated, infected family members.
Because about half of the world population is infected with H. pylori, antibacterial treatment for all people who are chronically infected may be impractical and could trigger antimicrobial resistance. Vaccination against H. pylori has been shown effective in experimental animal models, but thus far, such efficacy has not been studied in humans.
A randomized controlled trial (RCT) showed that short-term treatment with amoxicillin and omeprazole reduced the incidence of gastric cancer by 39% during a period of 15 years following randomization, with similar but not statistically significant reductions for gastric cancer mortality.
The magnitude of benefit of treating H. pylori in populations with different levels of gastric cancer risk has been unclear. A systematic review and meta-analysis of RCTs and observational studies was done to assess the treatment of H. pylori with curative regimens for three different clinical scenarios:
The authors found 24 eligible studies (22 from Asia) with 715 incident gastric cancers among 48,000 individuals in 340,000 person-years of follow-up. Individuals with eradication treatment for H. pylori had a lower incidence of gastric cancer (pooled incidence rate ratio, 0.53; 95% CI, 0.44–0.64). Treatment was associated with substantially lower risk in individuals who had asymptomatic infection (pooled incidence rate ratio, 0.62; 95% CI, 0.49–0.79) and in individuals after endoscopic resection of gastric cancer (pooled incidence rate ratio, 0.46; 95% CI, 0.35–0.60). Risk was not lower in those in the lowest tertile of gastric cancer incidence. Limitations of the study include a lack of consideration of the negative effects of treatment, such as causing antibiotic resistance of H. pylori and other microorganisms; and that eradication of H. pylori might reduce a postulated protective effect of H. pylori for esophageal adenocarcinoma. The results may have implications for the treatment of some subgroups of individuals with particularly high risk, such as Asian immigrant populations in the United States and individuals with underlying gastric mucosal disease (such as atrophic gastritis); or to help prevent recurrent gastric cancer.
Proton pump inhibitor (PPI) use is associated with worsening of gastric atrophy, particularly in H. pylori–infected individuals. One study analyzed 63,397 patients who were included in a territory-wide health database in Hong Kong, who had been treated for H. pylori between 2003 and 2012, and who had appeared to be cleared of the infection. The results suggested more than a twofold increase in risk of gastric cancer for those who used PPIs after H. pylori treatment, relative to those who had not used PPIs after H. pylori treatment. Because the finding could be caused by residual confounding or detection bias, its relevance to clinical practice is uncertain.
Interventions With Inadequate Evidence as to Whether They Reduce the Risk of Stomach (Gastric) Cancer or Evidence of No Effect
Excessive salt intake has been identified as a possible risk factor for gastric cancer in correlation and case-control studies. The daily intake of salt has decreased drastically in most western countries and in Japan, in part due to public health campaigns to reduce hypertensive diseases. This may be at least partially responsible for declines in gastric cancer rates. There is a consistent association between high salt intake and the risk of gastric cancer.
Epidemiologic evidence from case-control and cohort studies suggests that increased intake of fresh fruits and vegetables is associated with decreased gastric cancer rates.[23,24] However, no RCTs have been done to establish a causal association.
Because of the evidence for an inverse association between gastric cancer and dietary intake of fruits and vegetables, especially those rich in antioxidants, there has been interest in dietary supplementation with antioxidants.
Dietary indices of micronutrient intake have been calculated and indicate possible protective effects of beta carotene, vitamin A, vitamin E, selenium, vitamin C, or foods that contain these compounds. A chemoprevention trial in China reported a statistically significant reduction in the gastric cancer mortality rate after supplementation with beta carotene, vitamin E, and selenium. The population studied, however, may have been nutritionally deficient, raising questions of generalizability to other populations such as that of the United States. In addition, the experimental design did not permit assessment of the relative effects of beta carotene, vitamin E, and selenium.
Likewise, there was a randomized placebo-controlled trial of 200 mg of oral allitridium (a component of garlic) every day combined with 100 mcg of oral selenium every other day for 1 month of each year over a 3-year period in Qixia County (Shandong Province, China), an area with low intake of garlic and low selenium content in their garlic compared with other areas of China. Although designed as a double-blinded trial, allitridium causes a distinctive odor of garlic. A total of 5,033 people, who met at least one of the following criteria: (1) medical history of stomach disorder, (2) family history of tumor, (3) history of smoking, or (4) history of alcohol consumption, were randomly assigned. The study, published in a Chinese medical journal, was not well described. After a follow-up for as many as 11 years, there were a total of 23 gastric cancer cases in the allitridium/selenium group and 30 cases in the placebo group (relative risk [RR] after adjustment for a number of baseline characteristics = 0.48; 95% CI, 0.21–1.06). Only 60% of the gastric cancers were diagnosed by histopathology. There was a qualitative difference in outcome by sex: RRmen = 0.36 (95% CI, 0.14–0.92); RRwomen = 1.14 (95% CI, 0.22–5.76). Given the problems with design and reporting of the study, the evidence of benefit (including men) is weak and may not be generalizable to Western countries.
In a randomized, double-blind, chemoprevention trial in Venezuela among a population at increased risk for gastric cancer, a combination of antioxidant vitamins (vitamins C, E, and beta carotene) failed to modify progression or regression of precancerous gastric lesions. Another potential explanation for the lack of benefit of vitamin supplementation in this trial was the high prevalence of advanced premalignant lesions and the high H. pylori infection rate.
A secondary analysis of the Alpha-Tocopherol Beta Carotene trial conducted in male smokers in Finland evaluated the effect of supplementation on gastric cancer incidence. No protective effects for these supplements against gastric cancer were observed. Six-year follow-up results of a study of 976 Colombian patients have been reported. Patients were randomly assigned to receive eight different treatments that included vitamin supplements and anti-H. pylori therapy either alone or in combination versus placebo. Among the 79 patients who received anti-H. pylori therapy, a borderline statistically significant regression of intestinal metaplasia when compared with a placebo (15% vs. 6%; RR, 3.1; 95% CI, 1.0–9.3) was noted. However, the combinations of antibiotics and vitamins did not confer additional benefits. More importantly, the progression rate of intestinal metaplasia was comparable irrespective of the treatments received. The progression rate was 23% in the placebo group and 17% in antibiotic recipients.
A systematic review examined randomized trials of antioxidant dietary supplements for the prevention of gastrointestinal cancers, including gastric cancer. Twenty trials were identified that assessed the preventive effects of antioxidant supplements or vitamin C on gastrointestinal cancer. With regard to gastric cancer, there were 12 comparisons of one or more micronutrients with placebo: beta-carotene alone (4 trials); vitamin C alone (1 trial); vitamin E alone (1 trial); vitamin A plus beta-carotene (1 trial); beta-carotene plus vitamin C (1 trial); beta-carotene plus vitamin E (1 trial); beta-carotene plus vitamins C and E (1 trial); selenium plus vitamins C and E (1 trial); and beta-carotene, vitamins C and E, and selenium (1 trial). None of the comparisons showed a statistically significant effect on the incidence of gastric cancer. The overall summary estimate across all trials of antioxidants showed no statistically significant effect (RR of gastric cancer, 1.14; 95% CI, 0.97–1.33). Approximately 0.51% of participants in the combined antioxidant groups developed gastric cancer versus 0.38% in the placebo groups after treatment of 2.1 to 12 years and follow-up for as many as 14.1 years. In the combined analysis of all 20 trials of antioxidants for the prevention of gastrointestinal cancers, a fixed effects model showed an increase in overall mortality of antioxidants compared with a placebo (RR for mortality, 1.04; 95% CI, 1.02–1.07) but not in a random effects model (RR for mortality, 1.02; 95% CI, 0.97–1.07)
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
Added text to state that gastric cancer has been observed to be more common among individuals who use proton pump inhibitors (PPIs), relative to nonusers, after apparent successful Helicobacter pylori eradication therapy, but confounding and detection bias cannot be ruled out as explanations (cited Cheung et al. as reference 14).
Description of the Evidence
Added text to state that PPI use is associated with worsening of gastric atrophy, particularly in H. pylori–infected individuals. Also added text about one study that analyzed 63,397 patients who were included in a territory-wide health database in Hong Kong, who had been treated for H. pylori between 2003 and 2012, and who had appeared to be cleared of the infection; the results suggested more than a twofold increase in risk of gastric cancer for those who used PPIs after H. pylori treatment, relative to those who had not used PPIs after H. pylori treatment. Also added that because the finding could be caused by residual confounding or detection bias, its relevance to clinical practice is uncertain (cited Cheung et al. as reference 21).
This summary is written and maintained by the PDQ Screening and Prevention Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ® - NCI's Comprehensive Cancer Database pages.
Purpose of This Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about stomach (gastric) cancer prevention. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.
Reviewers and Updates
This summary is reviewed regularly and updated as necessary by the PDQ Screening and Prevention Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
Levels of Evidence
Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Screening and Prevention Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
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The preferred citation for this PDQ summary is:
PDQ® Screening and Prevention Editorial Board. PDQ Stomach (Gastric) Cancer Prevention. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: https://www.cancer.gov/types/stomach/hp/stomach-prevention-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389263]
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Last Revised: 2018-09-21
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