Stomach (Gastric) Cancer Prevention (PDQ®): Prevention - Health Professional Information [NCI]
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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.

Overview

Note: The Overview section summarizes the published evidence on this topic. The rest of the summary describes the evidence in more detail.

Other 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 older adults with atrophic gastritis or pernicious anemia; patients with sporadic gastric adenomas,[1] familial adenomatous polyposis,[2] or hereditary nonpolyposis colon cancer;[3] 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.[6]

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.[6] 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 mucosa-associated lymphatic tissue (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.[14] However, confounding and detection bias cannot be ruled out as explanations.

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%; I2 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; I2 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; I2 statistic, 55.0%) for studies with nonmatched pairs design. The proportion of EBV-associated gastric cancer among males was significantly higher than among females (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; I2 statistic, 0%) than among males (14.07; 95% CI, 10.46–18.93; I2 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).[15]

Compared with the general population, people with duodenal ulcer disease may have a lower risk of gastric cancer.[16]

Interventions for Reduction of Stomach (Gastric) Cancer Risk

Smoking cessation

Based on solid evidence, smoking is associated with an increased risk of stomach cancer.[17,18,19] 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.[20] 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.[17]

Study Design: Evidence obtained from case-control and cohort studies.
Internal Validity: Good.
Consistency: 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, suggested 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).[21] 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 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 after randomization.[22] With follow-up to 22 years, there was a reduction in both incidence and mortality.[23] A single-center randomized clinical trial in China included a total of 1,676 participants who were at higher risk of developing gastric cancer (elevated roughly threefold) because they had a first-degree relative with gastric cancer. Participants were randomly assigned to treatment with lansoprazole, amoxicillin, and clarithromycin or placebo for 7 days. After 9.2 years, this treatment regimen resulted in a reduction in gastric cancer, from 2.7% in the placebo group (23 individuals) to 1.2% in the treatment group (10 individuals), with a hazard ratio of 0.45 (95% CI, 0.21–0.94). No reduction in gastric cancer mortality was found, but the power to detect any difference was low.[24]

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.
Consistency: Good.
External Validity: Good.

Interventions With Inadequate Evidence as to Whether They Reduce the Risk of Stomach (Gastric) Cancer

Diet

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).

References:

  1. MING SC, GOLDMAN H: Gastric polyps: a histogenetic classification and its relation to carcinoma. Cancer 18: 721-6, 1965.
  2. Utsunomiya J, Maki T, Iwama T, et al.: Gastric lesion of familial polyposis coli. Cancer 34 (3): 745-54, 1974.
  3. Aarnio M, Salovaara R, Aaltonen LA, et al.: Features of gastric cancer in hereditary non-polyposis colorectal cancer syndrome. Int J Cancer 74 (5): 551-5, 1997.
  4. Kurtz RC, Sherlock P: The diagnosis of gastric cancer. Semin Oncol 12 (1): 11-8, 1985.
  5. Boeing H: Epidemiological research in stomach cancer: progress over the last ten years. J Cancer Res Clin Oncol 117 (2): 133-43, 1991.
  6. Pisters PWT, Kelsen DP, Tepper JE: Cancer of the stomach. In: DeVita VT Jr, Hellman S, Rosenberg SA, eds.: Cancer: Principles and Practice of Oncology. Vols. 1 & 2. 8th ed. Lippincott Williams & Wilkins, 2008, pp 1043-1079.
  7. Crew KD, Neugut AI: Epidemiology of gastric cancer. World J Gastroenterol 12 (3): 354-62, 2006.
  8. Leung WK, Wu MS, Kakugawa Y, et al.: Screening for gastric cancer in Asia: current evidence and practice. Lancet Oncol 9 (3): 279-87, 2008.
  9. Parsonnet J, Hansen S, Rodriguez L, et al.: Helicobacter pylori infection and gastric lymphoma. N Engl J Med 330 (18): 1267-71, 1994.
  10. Ando T, Goto Y, Maeda O, et al.: Causal role of Helicobacter pylori infection in gastric cancer. World J Gastroenterol 12 (2): 181-6, 2006.
  11. Aromaa A, Kosunen TU, Knekt P, et al.: Circulating anti-Helicobacter pylori immunoglobulin A antibodies and low serum pepsinogen I level are associated with increased risk of gastric cancer. Am J Epidemiol 144 (2): 142-9, 1996.
  12. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans: A review of human carcinogens--Part B: biological agents. Volume 100. IARC Press, 2011.
  13. Bouvard V, Baan R, Straif K, et al.: A review of human carcinogens--Part B: biological agents. Lancet Oncol 10 (4): 321-2, 2009.
  14. Cheung KS, Chan EW, Wong AYS, et al.: Long-term proton pump inhibitors and risk of gastric cancer development after treatment for Helicobacter pylori: a population-based study. Gut 67 (1): 28-35, 2018.
  15. Tavakoli A, Monavari SH, Solaymani Mohammadi F, et al.: Association between Epstein-Barr virus infection and gastric cancer: a systematic review and meta-analysis. BMC Cancer 20 (1): 493, 2020.
  16. Hansson LE, Nyrén O, Hsing AW, et al.: The risk of stomach cancer in patients with gastric or duodenal ulcer disease. N Engl J Med 335 (4): 242-9, 1996.
  17. Ladeiras-Lopes R, Pereira AK, Nogueira A, et al.: Smoking and gastric cancer: systematic review and meta-analysis of cohort studies. Cancer Causes Control 19 (7): 689-701, 2008.
  18. González CA, Pera G, Agudo A, et al.: Smoking and the risk of gastric cancer in the European Prospective Investigation Into Cancer and Nutrition (EPIC). Int J Cancer 107 (4): 629-34, 2003.
  19. La Torre G, Chiaradia G, Gianfagna F, et al.: Smoking status and gastric cancer risk: an updated meta-analysis of case-control studies published in the past ten years. Tumori 95 (1): 13-22, 2009 Jan-Feb.
  20. The Health Consequences of Smoking: A Report of the Surgeon General. U.S. Department of Health and Human Services, CDC, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Also available online. Last accessed March 28, 2024.
  21. Fuccio L, Zagari RM, Eusebi LH, et al.: Meta-analysis: can Helicobacter pylori eradication treatment reduce the risk for gastric cancer? Ann Intern Med 151 (2): 121-8, 2009.
  22. Ma JL, Zhang L, Brown LM, et al.: Fifteen-year effects of Helicobacter pylori, garlic, and vitamin treatments on gastric cancer incidence and mortality. J Natl Cancer Inst 104 (6): 488-92, 2012.
  23. Li WQ, Zhang JY, Ma JL, et al.: Effects of Helicobacter pylori treatment and vitamin and garlic supplementation on gastric cancer incidence and mortality: follow-up of a randomized intervention trial. BMJ 366: l5016, 2019.
  24. Choi IJ, Kim CG, Lee JY, et al.: Family History of Gastric Cancer and Helicobacter pylori Treatment. N Engl J Med 382 (5): 427-436, 2020.

Incidence and Mortality

Gastric cancer is the fifth most frequently diagnosed cancer and fourth leading cause of cancer-related mortality in the world,[1] although it is much rarer in the United States (1.3% of all new cancers).[2] The age-adjusted incidence rate for gastric cancer in the United States from 2016 to 2020 was 6.9 cases per 100,000 individuals. Incidence among men was nearly twice as high as among women.[3] Mortality rates for gastric cancer have been declining worldwide in recent decades, most prominently in the United States.[4,5] The mortality rate for White men in the United States was approximately 40 deaths per 100,000 men in 1930, compared with 3.3 deaths per 100,000 men for the years 2016 to 2020. The death rate from gastric cancer for Black men was 7.0 deaths per 100,000 men from 2016 to 2020.[3] The annual number of new cases seems to be steady in recent years. In 2024, it is estimated that 26,890 Americans will be diagnosed with gastric cancer and 10,880 persons will die of it.[2] Gastric cancer is the fifth most common cancer in the world.[6,7] Worldwide, the estimated number of cases per year in 2018 was 1,033,701, and the estimated number of deaths was 782,685. Age-standardized annual incidence rates vary widely across the world: from 4.7 to 32.1 cases per 100,000 in men, and from 3.0 to 13.2 cases per 100,000 in women. Incidence rates are markedly elevated in Eastern Asia.[7]

Most gastric cancers in the United States are advanced at diagnosis, which is reflected in an overall 5-year survival rate of 35.7% from 2013 to 2019.[3] 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.[8] 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. For more information, see Stomach (Gastric) Cancer Screening.

References:

  1. Sung H, Ferlay J, Siegel RL, et al.: Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries. CA Cancer J Clin 71 (3): 209-249, 2021.
  2. American Cancer Society: Cancer Facts and Figures 2024. American Cancer Society, 2024. Available online. Last accessed June 21, 2024.
  3. Surveillance Research Program, National Cancer Institute: SEER*Explorer: An interactive website for SEER cancer statistics. Bethesda, MD: National Cancer Institute. Available online. Last accessed March 6, 2024.
  4. Qiu D, Tanaka S: International comparisons of cumulative risk of stomach cancer, from Cancer Incidence in Five Continents Vol. VIII. Jpn J Clin Oncol 36 (2): 123-4, 2006.
  5. Stomach. In: Ries LA, Kosary CL, Hankey BF, et al., eds.: SEER Cancer Statistics Review 1973-1995. National Cancer Institute, 1998, Section 13.
  6. Parkin DM: Global cancer statistics in the year 2000. Lancet Oncol 2 (9): 533-43, 2001.
  7. Bray F, Ferlay J, Soerjomataram I, et al.: Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin 68 (6): 394-424, 2018.
  8. Tan YK, Fielding JW: Early diagnosis of early gastric cancer. Eur J Gastroenterol Hepatol 18 (8): 821-9, 2006.

Pathogenesis

Understanding of 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.[1] 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.

References:

  1. Correa P: Human gastric carcinogenesis: a multistep and multifactorial process--First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention. Cancer Res 52 (24): 6735-40, 1992.

Interventions for Reduction of Stomach (Gastric) Cancer Risk

Smoking Cessation

Studies have shown that smoking is a key risk factor for gastric cancer. 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.[1] Another systematic review of studies addressed the relationship between cigarette smoking and gastric cancer by estimating the magnitude of the association for different levels of exposure to cancer. It provides solid evidence that smoking is the most important behavioral risk factor for gastric cancer.[1,2,3] The risk of stomach cancer decreases among former smokers, compared with persistent 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

Helicobacter pylori infection is an accepted cause of gastric adenocarcinoma.[4,5] Questions remain concerning the natural history of H. pylori infection, and the mechanism of transmission and the rates of reinfection or recrudescence for different populations are unknown.[6,7] A small randomized trial of antibiotic eradication in 140 H. pylori-infected people suggested the possibility of transmission among close family members.[8] 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. Such efficacy has not been studied in humans.

A randomized controlled trial (RCT) of 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.[9] With follow-up to 22 years, H. pylori treatment was associated with an absolute reduction in the risk of gastric cancer death of 16 cases per 1,000 individuals. For vitamin supplementation, the absolute risk reduction was 19 cases per 1,000 individuals; for garlic supplementation, it was 10 cases per 1,000 individuals. H. pylori treatment and vitamin supplementation were also associated with absolute reductions in gastric cancer incidence of 33 cases and 19 cases per 1,000 individuals, respectively.[10]

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 assessed the treatment of H. pylori with curative regimens for three different clinical scenarios:[11]

  • Asymptomatic patients.
  • Patients with atrophic gastritis and intestinal metaplasia.
  • Patients who have had endoscopic treatment for cancer (who usually have remaining advanced atrophic gastritis and are, therefore, at high future risk).

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 a 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 included a lack of consideration of the negative effects of treatment, such as antibiotic resistance of H. pylori and other microorganisms. In addition, 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 at particularly high risk for stomach cancer, such as Asian immigrant populations in the United States and individuals with underlying gastric mucosal disease such as atrophic gastritis. The results may also have implications for the prevention of recurrent gastric cancer.[11]

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. These patients had been treated for H. pylori between 2003 and 2012 and 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 did not use PPIs after H. pylori treatment.[12] Because the finding could be caused by residual confounding or detection bias, its relevance to clinical practice is uncertain.

References:

  1. Ladeiras-Lopes R, Pereira AK, Nogueira A, et al.: Smoking and gastric cancer: systematic review and meta-analysis of cohort studies. Cancer Causes Control 19 (7): 689-701, 2008.
  2. González CA, Pera G, Agudo A, et al.: Smoking and the risk of gastric cancer in the European Prospective Investigation Into Cancer and Nutrition (EPIC). Int J Cancer 107 (4): 629-34, 2003.
  3. La Torre G, Chiaradia G, Gianfagna F, et al.: Smoking status and gastric cancer risk: an updated meta-analysis of case-control studies published in the past ten years. Tumori 95 (1): 13-22, 2009 Jan-Feb.
  4. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans: A review of human carcinogens--Part B: biological agents. Volume 100. IARC Press, 2011.
  5. Bouvard V, Baan R, Straif K, et al.: A review of human carcinogens--Part B: biological agents. Lancet Oncol 10 (4): 321-2, 2009.
  6. Cheung TK, Xia HH, Wong BC: Helicobacter pylori eradication for gastric cancer prevention. J Gastroenterol 42 (Suppl 17): 10-5, 2007.
  7. de Vries AC, Haringsma J, Kuipers EJ: The detection, surveillance and treatment of premalignant gastric lesions related to Helicobacter pylori infection. Helicobacter 12 (1): 1-15, 2007.
  8. Sari YS, Can D, Tunali V, et al.: H pylori: Treatment for the patient only or the whole family? World J Gastroenterol 14 (8): 1244-7, 2008.
  9. Ma JL, Zhang L, Brown LM, et al.: Fifteen-year effects of Helicobacter pylori, garlic, and vitamin treatments on gastric cancer incidence and mortality. J Natl Cancer Inst 104 (6): 488-92, 2012.
  10. Li WQ, Zhang JY, Ma JL, et al.: Effects of Helicobacter pylori treatment and vitamin and garlic supplementation on gastric cancer incidence and mortality: follow-up of a randomized intervention trial. BMJ 366: l5016, 2019.
  11. Lee YC, Chiang TH, Chou CK, et al.: Association Between Helicobacter pylori Eradication and Gastric Cancer Incidence: A Systematic Review and Meta-analysis. Gastroenterology 150 (5): 1113-1124.e5, 2016.
  12. Cheung KS, Chan EW, Wong AYS, et al.: Long-term proton pump inhibitors and risk of gastric cancer development after treatment for Helicobacter pylori: a population-based study. Gut 67 (1): 28-35, 2018.

Interventions With Inadequate Evidence as to Whether They Reduce the Risk of Stomach (Gastric) Cancer or Evidence of No Effect

Diet

Excessive salt intake has been identified as a possible risk factor for gastric cancer in correlation and case-control studies.[1] 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.

Epidemiological evidence from case-control and cohort studies suggests that increased intake of fresh fruits and vegetables is associated with decreased gastric cancer rates.[2,3] However, no randomized controlled trials have been done to establish a causal association.

Dietary Supplements

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.[4] 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 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. The study took place 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.[5] Although designed as a double-blinded trial, researchers noted that allitridum causes a distinctive garlic odor. Investigators randomly assigned 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. The study, published in a Chinese medical journal, was not well described. After a follow-up of up to 11 years, there were 23 gastric cancer cases in the allitridum/selenium group and 30 cases in the placebo group (relative risk [RR] after adjustment for several baseline characteristics, 0.48; 95% confidence interval [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) was 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.[6] 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 Helicobacter pylori infection rate.[7]

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.[8] 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 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 regardless of the treatments received. The progression rate was 23% in the placebo group and 17% in antibiotic recipients.[9]

A systematic review examined randomized trials of antioxidant dietary supplements for the prevention of gastrointestinal cancers, including gastric cancer.[10] 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). After treatment of 2.1 to 12 years and follow-up for as many as 14.1 years, approximately 0.51% of participants in the combined antioxidant groups developed gastric cancer versus 0.38% in the placebo groups. 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 for antioxidants compared with placebo (RR for mortality, 1.04; 95% CI, 1.02–1.07). A random effects model showed no such increase (RR for mortality, 1.02; 95% CI, 0.97–1.07).

References:

  1. D'Elia L, Galletti F, Strazzullo P: Dietary salt intake and risk of gastric cancer. Cancer Treat Res 159: 83-95, 2014.
  2. Buiatti E, Palli D, Decarli A, et al.: A case-control study of gastric cancer and diet in Italy: II. Association with nutrients. Int J Cancer 45 (5): 896-901, 1990.
  3. Pisters PWT, Kelsen DP, Tepper JE: Cancer of the stomach. In: DeVita VT Jr, Hellman S, Rosenberg SA, eds.: Cancer: Principles and Practice of Oncology. Vols. 1 & 2. 8th ed. Lippincott Williams & Wilkins, 2008, pp 1043-1079.
  4. Blot WJ, Li JY, Taylor PR, et al.: Nutrition intervention trials in Linxian, China: supplementation with specific vitamin/mineral combinations, cancer incidence, and disease-specific mortality in the general population. J Natl Cancer Inst 85 (18): 1483-92, 1993.
  5. Li H, Li HQ, Wang Y, et al.: An intervention study to prevent gastric cancer by micro-selenium and large dose of allitridum. Chin Med J (Engl) 117 (8): 1155-60, 2004.
  6. Plummer M, Vivas J, Lopez G, et al.: Chemoprevention of precancerous gastric lesions with antioxidant vitamin supplementation: a randomized trial in a high-risk population. J Natl Cancer Inst 99 (2): 137-46, 2007.
  7. Taylor PR: Prevention of gastric cancer: a miss. J Natl Cancer Inst 99 (2): 101-3, 2007.
  8. Malila N, Taylor PR, Virtanen MJ, et al.: Effects of alpha-tocopherol and beta-carotene supplementation on gastric cancer incidence in male smokers (ATBC Study, Finland). Cancer Causes Control 13 (7): 617-23, 2002.
  9. Correa P, Fontham ET, Bravo JC, et al.: Chemoprevention of gastric dysplasia: randomized trial of antioxidant supplements and anti-helicobacter pylori therapy. J Natl Cancer Inst 92 (23): 1881-8, 2000.
  10. Bjelakovic G, Nikolova D, Simonetti RG, et al.: Antioxidant supplements for preventing gastrointestinal cancers. Cochrane Database Syst Rev (3): CD004183, 2008.

Latest Updates to This Summary (03 / 19 / 2024)

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.

Incidence and Mortality

Updated statistics with estimated new cases and deaths for 2024 (cited American Cancer Society as reference 2).

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® Cancer Information for Health Professionals pages.

About This PDQ Summary

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:

  • be discussed at a meeting,
  • be cited with text, or
  • replace or update an existing article that is already cited.

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

PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as "NCI's PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary]."

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]

Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.

Disclaimer

The information in these summaries should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.

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More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website's Email Us.

Last Revised: 2024-03-19

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