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,[
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.[
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.[
There is consistent and solid evidence that Epstein-Barr virus (EBV) infection is strongly associated with gastric cancer. A systematic review and meta-analysis of 71 articles (4 from the United States) assessed the prevalence and association of EBV and gastric cancer. EBV infection was associated with a large increase in gastric cancer risk. The pooled prevalence of EBV in 20,361 patients with gastric cancer was 8.77% (95% confidence interval [CI], 7.73%–9.92%; I 2 statistic, 83.2%). Results were consistent across studies, although heterogenous. The pooled odds ratios (ORs) for gastric cancer were 18.56 (95% CI, 15.68–21.97; I 2 statistic, 55.4%) for studies (kappa statistic, 20; n = 4,116 patients with cancer) with matched pairs design (including tumor and tumor-adjacent normal tissues) and 3.31 (95% CI, 0.95–11.54; I 2 statistic, 55.0%) for studies with nonmatched pairs design. The proportion of EBV-associated gastric cancer among male cases was significantly higher than among female cases (10.8% vs. 5.7%) (P < .0001). However, the pooled OR estimate for EBV-associated gastric cancer was significantly higher among females (21.47; 95% CI, 15.55–29.63; I 2 statistic, 0%) than among males (14.07; 95% CI, 10.46–18.93; I 2 statistic, 49.0%) (P = .06). EBV was more prevalent in the cardia (12.5%) and the body (11.7%) compared with the antrum (6.3%) (P = .0002).[
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.[
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.[
|Study Design: Evidence obtained from case-control and cohort studies.|
|Internal Validity: Good.|
|External Validity: Good.|
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% CI, 0.43–0.98).[
In the initial report from a randomized clinical trial, 3,365 participants were followed in an intention-to-treat analysis. Short-term treatment with amoxicillin and omeprazole was associated with a 39% reduction in gastric cancer incidence during a period of 15 years following randomization.[
Magnitude of Effect: Risk of gastric cancer and gastric cancer mortality may be reduced.
|Study Design: Randomized controlled trials of H. pylori eradication.|
|Internal Validity: Good.|
|External Validity: Good.|
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.
|Study Design: Cohort or case-control studies.|
|Internal Validity: Good.|
|Consistency: Small number of studies.|
|External Validity: Fair (populations vary greatly in their underlying nutritional status).|
Gastric cancer is the fifth most frequently diagnosed cancer and third leading cause of cancer-related mortality in the world, although it is much rarer in the United States (1.4% of all new cancers).[
Most gastric cancers in the United States are advanced at diagnosis, which is reflected in an overall 5-year survival rate of 32.2% from 2010 to 2016.[
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.[
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
Helicobacter pylori infection is an accepted cause of gastric adenocarcinoma.[
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) that involved 3,365 participants from a nutritionally deprived population 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.[
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.[
Excessive salt intake has been identified as a possible risk factor for gastric cancer in correlation and case-control studies.[
Epidemiologic evidence from case-control and cohort studies suggests that increased intake of fresh fruits and vegetables is associated with decreased gastric cancer rates.[
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.[
Likewise, there was a randomized placebo-controlled trial of 200 mg of oral allitridum (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.[
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.[
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.[
A systematic review examined randomized trials of antioxidant dietary supplements for the prevention of gastrointestinal cancers, including gastric cancer.[
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 there is consistent and solid evidence that Epstein-Barr virus (EBV) infection is strongly associated with gastric cancer; a systematic review and meta-analysis of 71 articles assessed the prevalence and association of EBV and gastric cancer and found that EBV infection was associated with a large increase in gastric cancer risk. Results were consistent across studies, although heterogenous, and EBV was more prevalent in the cardia and the body compared with the antrum (cited Tavakoli et al. as reference 15).
Incidence and Mortality
Added text to state that gastric cancer is the fifth most frequently diagnosed cancer and third leading cause of cancer-related mortality in the world, although it is much rarer in the United States (cited Tavakoli et al. as reference 1). Also updated statistics with estimated new cases and deaths for 2022 (cited American Cancer Society as reference 5).
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 in the care of their 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.
Permission to Use This Summary
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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: 2022-02-07
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