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

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 Prevention; Gastric Cancer Treatment; and Levels of Evidence for Cancer Screening and Prevention Studies are also available.

Inadequate Evidence of Benefit Associated With Screening

Barium-meal gastric photofluorography and serum pepsinogen

Based on fair evidence, screening with barium-meal photofluorography or serum pepsinogen would not result in a decrease in mortality from gastric cancer in areas with relatively low incidence of the disease, such as the United States.[1,2,3,4]

Magnitude of Effect: Fair evidence for no reduction in mortality.

Gastric endoscopy

Magnitude of Effect: Inadequate evidence for mortality reduction.

Harms

Based on solid evidence, screening would result in uncommon but serious side effects associated with endoscopy, which may include perforation, cardiopulmonary events, aspiration pneumonia, and bleeding requiring hospitalization.

Magnitude of Effect: Solid evidence for rare but serious harms.

References:

1. Hirayama T, Hisamichi S, Fujimoto I, et al.: Screening for gastric cancer. In: Miller AB, ed.: Screening for Cancer. Academic Press, 1985, pp 367-376.
2. Tytgat GN, Mathus-Vliegen EM, Offerhaus J: Value of endoscopy in the surveillance of high-risk groups for gastrointestinal cancer. In: Sherlock P, Morson BC, Barbara L, et al., eds.: Precancerous Lesions of the Gastrointestinal Tract. Raven Press, 1983, pp 305-318.
3. Riecken B, Pfeiffer R, Ma JL, et al.: No impact of repeated endoscopic screens on gastric cancer mortality in a prospectively followed Chinese population at high risk. Prev Med 34 (1): 22-8, 2002.
4. Kitahara F, Kobayashi K, Sato T, et al.: Accuracy of screening for gastric cancer using serum pepsinogen concentrations. Gut 44 (5): 693-7, 1999.
5. 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.

Incidence and Mortality

In 2024, it is estimated that 26,890 Americans will be diagnosed with gastric cancer and 10,880 will die of it.[1] Two-thirds of people diagnosed with gastric cancer are older than 66 years. Gastric cancer is the fourth most common cause of cancer mortality in the world. The disease is common in places such as East Asia, South-Central Asia, South and Central America, and Eastern Europe. Gastric cancer is a major cause of death worldwide.[2]

The major type of gastric cancer is adenocarcinoma (95%). The remaining malignant tumors include lymphomas, sarcomas, carcinoid tumors, and other rare types. Distinguishing the common adenocarcinoma from the uncommon lymphoma may sometimes be difficult, but it is important because of major differences in staging, treatment, and prognosis.[3] Gastric adenocarcinomas can be further categorized into an intestinal type and a diffuse type.[4] Intestinal-type lesions are frequently ulcerative and occur in the distal stomach more often than the diffuse type. Diffuse-type lesions are associated with a worse prognosis than the intestinal type. The intestinal type tends to be predominant in geographic regions with a high incidence of gastric carcinoma. The decline in the incidence of gastric cancer worldwide largely results from a decrease in the number of intestinal-type lesions.[5]

References:

1. American Cancer Society: Cancer Facts and Figures 2024. American Cancer Society, 2024. Available online. Last accessed June 21, 2024.
2. 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.
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. Lauren P: The two histological main types of gastric carcinoma: diffuse and so-called intestinal-type carcinoma: an attempt at a histo-clinical classification. Acta Pathol Microbiol Scand 64(1): 31-49, 1965.
5. Henson DE, Dittus C, Younes M, et al.: Differential trends in the intestinal and diffuse types of gastric carcinoma in the United States, 1973-2000: increase in the signet ring cell type. Arch Pathol Lab Med 128 (7): 765-70, 2004.

Risk Factors

The incidence of gastric cancer in the United States has decreased fourfold since 1930, to approximately seven cases per 100,000 people.[1] The reasons for this striking decrease in incidence are not fully understood but are suspected to be related to improved storage of food and changes in diet, such as decreased salt intake. Some populations of Americans are at elevated risk, including older patients with atrophic gastritis or pernicious anemia; patients with sporadic gastric adenomas,[2] familial adenomatous polyposis,[3] or hereditary nonpolyposis colon cancer;[4] and immigrant ethnic populations from countries with high rates of gastric carcinoma.[5,6]

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 and environmental factors include a family history of gastric cancer; low consumption of fruits and vegetables; consumption of salted, smoked, or poorly preserved foods; and cigarette smoking.[7,8] There is consistent evidence that Helicobacter 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 (IARC) classifies H. pylori infection as a cause of noncardia gastric carcinoma and low-grade B-cell mucosa-associated lymphatic tissue gastric lymphoma (i.e., a Group 1 human carcinogen).[12,13] Compared with the general population, people with duodenal ulcer disease may have a lower risk of gastric cancer.[14]

References:

1. National Cancer Institute: SEER Stat Fact Sheets: Stomach Cancer. Bethesda, Md: National Cancer Institute. Available online. Last accessed March 19, 2024.
2. MING SC, GOLDMAN H: Gastric polyps: a histogenetic classification and its relation to carcinoma. Cancer 18: 721-6, 1965.
3. Utsunomiya J, Maki T, Iwama T, et al.: Gastric lesion of familial polyposis coli. Cancer 34 (3): 745-54, 1974.
4. 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.
5. Kurtz RC, Sherlock P: The diagnosis of gastric cancer. Semin Oncol 12 (1): 11-8, 1985.
6. Boeing H: Epidemiological research in stomach cancer: progress over the last ten years. J Cancer Res Clin Oncol 117 (2): 133-43, 1991.
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. 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.

Inadequate Evidence of Benefit Associated With Screening

Several screening techniques, including barium-meal photofluorography, gastric endoscopy, and serum pepsinogen, have been proposed as screening methods for the early detection of gastric cancer. No randomized trials evaluating the impact of screening on mortality from gastric cancer have been reported.[1,2] Even in very high-risk areas, the positive predictive value (PPV) of the screening tests may be very low. In a screening program of 17,647 men aged 40 to 60 years in Wakayama City, Japan, the PPV of combined serum pepsinogen and barium meal with digital radiography over the 7-year period was 0.85%.[3] The positive test rates were 19.5% for serum pepsinogen and 22.5% for radiography, with a cancer detection rate of 0.28%. Over the 7-year period, there was no reduction in gastric cancer mortality compared with an age-matched surrounding population.

Barium-Meal Gastric Photofluorography

A national program of population-based screening for gastric cancer using barium-meal photofluorography has been ongoing since the 1960s in Japan. Participation rates have been in the range of only 10% to 20%.[1,3] Although there has been a coincident decrease in mortality from gastric cancer in Japan, mortality rates have been decreasing in many developed countries without screening programs. Case-control studies from Japan show decreases in gastric mortality in people who have undergone screening, but results from prospective studies were not consistent.[1,2]

A pilot study of community-based photofluorography was conducted in Costa Rica using the same techniques as those used in Japan's national program (with consultation from Japanese experts).[4] People were invited by letter from a population registry to attend two rounds of screening, and a total of 6,200 eligible screened participants (of a planned 12,000) were analyzed. Their gastric cancer mortality from 2 to 7 years after screening was compared with four control groups that had not been invited to be screened, and the relative risk was about 0.5 (no P value reported). The study was, however, prone to strong biases, including selection bias, and likely differential exclusion of people with previously diagnosed gastric cancer favoring the screened population. In addition, unlike the community controls, patients diagnosed with gastric cancer through the screening program were treated at a single referral center. The PPV of a suspicious fluorograph was 3%; the specificity in the two rounds was 67% and 80%; and the positivity rates were 34% and 20%. Despite the authors' belief that their results provided substantial evidence that routine screening would decrease gastric cancer mortality, they concluded that the costs of screening with photofluorography would be far too high in their country.

A screening study was begun in Venezuela in 1980, using radiographic fluorography.[5] The efficacy of this program in reducing mortality from gastric cancer was evaluated by means of a case-control study. The study showed no detectable reduction in mortality from gastric cancer.

Gastric Endoscopy

Endoscopy appears to be more sensitive than photofluorography for the detection of gastric cancer.[6]

A meta-analysis of gastric cancer endoscopic screening studies in Asia identified ten relevant studies, all nonrandomized.[7] These studies were conducted between 1989 and 2014 in South Korea, China, and Japan. Of the ten studies, a never-screened group was the comparator in six studies, a radiographic-screening group was the comparator in one study, and expected deaths based on population rates was the comparator in three studies. In some of the studies, the endoscopic screening was performed as part of a national screening program. The meta-analysis pooled risk ratio (RR) estimate of gastric cancer mortality associated with endoscopic screening was 0.60 (95% confidence interval [CI], 0.49–0.73), with all but one study showing an individual RR of 0.72 or lower. There was significant heterogeneity across studies (P = .001), which was because of the one study with an RR greater than 1 (1.01); removing that study resulted in no significant heterogeneity (P = .14). Pooled estimates for the four nested case-control studies and six cohort studies were 0.60 (95% CI, 0.47–0.76) and 0.57 (95% CI, 0.39–0.83), respectively. The pooled estimate for the six studies with the never-screened comparator group was 0.58 (95% CI, 0.48–0.70).

Serum Pepsinogen

There are no studies evaluating the effect of screening with serum pepsinogen on gastric cancer mortality, and there are important limitations to its use as a screening test. Low serum pepsinogen levels indicate the presence of atrophic gastritis and are therefore applicable to the detection of presumed precursors for intestinal-type gastric cancer rather than the diffuse type.[3] In addition, there are no standard cut-off values of abnormality.[1,8] Finally, eradication of H. pylori and use of proton pump inhibitors for the management of indigestion change pepsinogen levels, making interpretation of results difficult in the setting of widespread use of these interventions.[1,3]

In Japan, one study measured serum pepsinogen levels I and II (PGI and PGII) in 5,113 patients who were also screened by endoscopy (13 gastric cancers detected). This study used cut-off points for identifying risk of gastric cancer, which were less than 70 ng/mL for PGI and less than 3 ng/mL for the PGI:PGII ratio. This combination provided a sensitivity of 84.6%, a specificity of 73.5%, a PPV of 0.81%, and a negative predictive value of 99.6%.[9]

Clinical Considerations for High-Risk Groups

There may be justification for screening some populations of Americans at higher risk, although there is considerable discussion about how much incidence would make the examination worthwhile. Potential subgroups might include older patients with atrophic gastritis or pernicious anemia; patients with partial gastrectomy;[10] patients with the diagnosis of sporadic adenomas,[11] familial adenomatous polyposis,[12] or hereditary nonpolyposis colon cancer;[13] and immigrant ethnic populations from countries with high rates of gastric carcinoma.[14,15]

References:

1. 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.
2. Hamashima C, Shibuya D, Yamazaki H, et al.: The Japanese guidelines for gastric cancer screening. Jpn J Clin Oncol 38 (4): 259-67, 2008.
3. Ohata H, Oka M, Yanaoka K, et al.: Gastric cancer screening of a high-risk population in Japan using serum pepsinogen and barium digital radiography. Cancer Sci 96 (10): 713-20, 2005.
4. Rosero-Bixby L, Sierra R: X-ray screening seems to reduce gastric cancer mortality by half in a community-controlled trial in Costa Rica. Br J Cancer 97 (7): 837-43, 2007.
5. Pisani P, Oliver WE, Parkin DM, et al.: Case-control study of gastric cancer screening in Venezuela. Br J Cancer 69 (6): 1102-5, 1994.
6. Tashiro A, Sano M, Kinameri K, et al.: Comparing mass screening techniques for gastric cancer in Japan. World J Gastroenterol 12 (30): 4873-4, 2006.
7. Zhang X, Li M, Chen S, et al.: Endoscopic Screening in Asian Countries Is Associated With Reduced Gastric Cancer Mortality: A Meta-analysis and Systematic Review. Gastroenterology 155 (2): 347-354.e9, 2018.
8. Yanaoka K, Oka M, Mukoubayashi C, et al.: Cancer high-risk subjects identified by serum pepsinogen tests: outcomes after 10-year follow-up in asymptomatic middle-aged males. Cancer Epidemiol Biomarkers Prev 17 (4): 838-45, 2008.
9. Kitahara F, Kobayashi K, Sato T, et al.: Accuracy of screening for gastric cancer using serum pepsinogen concentrations. Gut 44 (5): 693-7, 1999.
10. Staël von Holstein C, Eriksson S, Huldt B, et al.: Endoscopic screening during 17 years for gastric stump carcinoma. A prospective clinical trial. Scand J Gastroenterol 26 (10): 1020-6, 1991.
11. MING SC, GOLDMAN H: Gastric polyps: a histogenetic classification and its relation to carcinoma. Cancer 18: 721-6, 1965.
12. Utsunomiya J, Maki T, Iwama T, et al.: Gastric lesion of familial polyposis coli. Cancer 34 (3): 745-54, 1974.
13. 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.
14. Kurtz RC, Sherlock P: The diagnosis of gastric cancer. Semin Oncol 12 (1): 11-8, 1985.
15. Boeing H: Epidemiological research in stomach cancer: progress over the last ten years. J Cancer Res Clin Oncol 117 (2): 133-43, 1991.

Evidence of Harm Associated With Screening

Harms of routine screening for gastric cancer are poorly quantitated or reported and derive chiefly from screening experiences in very high-risk areas such as Japan.[1] The most frequent harm is the occurrence of false-positive tests.[2] Exposure to the low doses of radiation (about 0.6 mSv in photofluorography) carries a theoretical but poorly quantified risk of carcinogenesis. Additional rare complications of screening may include adverse effects of premedication (used for endoscopy and sometimes photofluorography) and bleeding or perforation from endoscopy.[1] As with any screening test, there is a possibility of overdiagnosis with attendant overtreatment. Since harms such as perforation and bleeding may vary with the experience of the screening center, the harms may be higher in populations at low risk for gastric cancer, such as the United States, than in mass screening programs in Japan.

References:

1. Hamashima C, Shibuya D, Yamazaki H, et al.: The Japanese guidelines for gastric cancer screening. Jpn J Clin Oncol 38 (4): 259-67, 2008.
2. Ohata H, Oka M, Yanaoka K, et al.: Gastric cancer screening of a high-risk population in Japan using serum pepsinogen and barium digital radiography. Cancer Sci 96 (10): 713-20, 2005.

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 1).

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 screening. 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.

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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).

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PDQ® Screening and Prevention Editorial Board. PDQ Stomach (Gastric) Cancer Screening. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: https://www.cancer.gov/types/stomach/hp/stomach-screening-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389174]

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Last Revised: 2024-03-19