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Table of Contents Purpose of This PDQ Summary
Summary of Evidence
Significance
Evidence of Benefit
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Changes To This Summary (02/29/2008)
Questions or Comments About This Summary
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Purpose of This PDQ Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about gastric cancer screening. This summary is reviewed regularly and updated as necessary by the PDQ Screening and Prevention Editorial Board.
Information about the following is included in this summary:
- Gastric cancer incidence and mortality statistics and information about gastric cancer risk factors.
- Gastric cancer screening modalities.
- Benefits and harms of gastric cancer screening.
This summary is intended as a resource to inform clinicians and other health professionals about currently available gastric cancer screening modalities. The PDQ Screening and Prevention Editorial Board uses a formal evidence ranking system in reporting the evidence of benefit and potential harms associated with each screening modality. It does not provide formal guidelines or recommendations for making health care decisions. Information in this summary should not be used as a basis for reimbursement determinations.
This summary is also available in a patient version, which is written in less technical language.
Back to Top Summary of Evidence
Note: Separate PDQ summaries on Stomach (Gastric) Cancer Prevention, Gastric Cancer
Treatment, and Levels of Evidence for Cancer Screening and Prevention Studies are also available.
Benefits
Based on fair evidence, screening would not result in a decrease in mortality from gastric cancer in the U.S. population.
Description of the Evidence
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Study Design: Evidence obtained from case-control studies.
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Internal Validity: Fair.
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Consistency: Multiple studies, large number of participants.
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Magnitude of Effects on Health Outcomes: Fair evidence for no reduction in mortality.
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External Validity: Fair.
Harms
Based on solid evidence, endoscopic screening would result in uncommon but serious side effects associated with endoscopy, which may include perforation, cardiopulmonary events, aspiration pneumonia, and bleeding requiring hospitalization.
Description of the Evidence
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Study Design: Evidence obtained from well-designed and conducted case-control studies.
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Internal Validity: Fair.
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Consistency: Multiple studies, large number of participants.
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Magnitude of Effects on Health Outcomes: Good evidence for rare but serious harms.
Back to Top Significance
Natural History, Incidence, and Mortality
Gastric cancer is the 14th most frequent cause of cancer mortality in the United States. In 2008, it is estimated that 21,500 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. The disease is much more common
in other countries, principally Japan, Central Europe, Scandinavia, Hong Kong,
South and Central America, the Soviet Union, China, and Korea. Gastric cancer is
a major cause of death worldwide, especially in developing countries.[2] The
major type of gastric cancer is adenocarcinoma (90%). The remaining 10%
include lymphomas, sarcomas, and other rare types.[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
predominate in geographic regions with a high incidence of gastric carcinoma.
The decline in the incidence of gastric cancer worldwide is largely due to a
decrease in the number of intestinal type lesions.
Risk Factors
The incidence of gastric cancer in the United States has decreased fourfold since
1930 to approximately seven cases per 100,000 people. The reasons for this
striking decrease in incidence are unknown but are suspected to be related to
improved storage of food, or changes in diet such as decreased salt intake.
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.[5] There is increasing evidence that Helicobacter pylori
infection of the stomach is associated with both the initiation and promotion
of gastric carcinoma and gastric lymphoma.[6-8] Compared with the general population,
people with duodenal ulcer disease may have a lower risk of gastric cancer.[9]
There is considerable dispute as to whether partial gastrectomy, especially
Billroth II gastrectomy for benign causes, increases risk.[10,11]
References
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American Cancer Society.: Cancer Facts and Figures 2008. Atlanta, Ga: American Cancer Society, 2008. Also available online. Last accessed October 1, 2008.
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American Cancer Society.: Cancer Facts and Figures 2005. Atlanta, Ga: American Cancer Society, 2005. Also available online. Last accessed July 31, 2008.
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Fine G, Chan K: Alimentary tract. In: Kissane JM, ed.: Anderson's Pathology. Vol 2. 8th ed. Saint Louis, Mo: CV Mosby, 1985, pp 1055-1095.
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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.
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Crew KD, Neugut AI: Epidemiology of gastric cancer. World J Gastroenterol 12 (3): 354-62, 2006.
[PUBMED Abstract]
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Parsonnet J, Hansen S, Rodriguez L, et al.: Helicobacter pylori infection and gastric lymphoma. N Engl J Med 330 (18): 1267-71, 1994.
[PUBMED Abstract]
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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.
[PUBMED Abstract]
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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.
[PUBMED Abstract]
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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.
[PUBMED Abstract]
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Schafer LW, Larson DE, Melton LJ 3rd, et al.: The risk of gastric carcinoma after surgical treatment for benign ulcer disease. A population-based study in Olmsted County, Minnesota. N Engl J Med 309 (20): 1210-3, 1983.
[PUBMED Abstract]
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Greene FL: Neoplastic changes in the stomach after gastrectomy. Surg Gynecol Obstet 171 (6): 477-80, 1990.
[PUBMED Abstract]
Back to Top Evidence of Benefit
Gastroscopic examination has been proposed as a screening method for the early detection of gastric cancer. No randomized trials evaluating the impact of screening on mortality from gastric cancer have been reported, although a Japanese study randomizing municipalities within a prefecture is ongoing.[1]
Time-trend analysis and case-control studies of gastric endoscopy suggest a twofold decrease in gastric cancer mortality in screened versus unscreened individuals;[2-6] however, this stands in contrast to studies of stronger design.
A cohort study of 24,134 individuals with a follow-up period of 40 months did not demonstrate a statistically significant decrease in gastric cancer mortality among men or women who were screened compared with those who were not screened.[7] A larger prospective study examined the association between screening in the past 12 months and subsequent gastric cancer mortality and other-cause mortality. The risk of death from gastric cancer and from causes of death other than gastric cancer were reduced among those who had participated in gastric cancer screening programs, demonstrating a selection for healthier individuals into screening programs.[8]
Another cohort study was conducted in Linqu County, China, where gastric cancer rates are high, in which over 4,000 adult residents were screened. Individuals were screened at an average of 4.5 year intervals, except for a high-risk subset (689 individuals) that was screened 2 years after the initial examination. Of the 85 cases of gastric cancer occurring in the cohort, 58 were detected with screening. No impact on gastric cancer mortality was observed among screened individuals. The standardized mortality ratio (SMR) for gastric cancer 10 years after the initial screen was 1.01 (95% confidence interval, 0.72–1.37). The SMR for all-cause mortality was significantly lower among participants since individuals with hypertension, liver disease, and chronic obstructive pulmonary disease were not eligible to participate.[9] The study was not designed to evaluate screening, and the intervals between screens were long.
A screening study was begun in Venezuela in 1980, using radiographic fluorography.[10] The efficacy of this program in reducing mortality from stomach cancer was evaluated by means of a case-control study. Analyses determined that the tests were ineffective in reducing mortality from gastric cancer.
In Japan, measurement of serum pepsinogen (PGI and PGII) levels in 5,113 subjects also screened by endoscopy (13 gastric cancers detected), used cut-off points for identifying risk for gastric cancer of less than 70 ng/mL for pepsinogen I and less than 3 for the PGI:PGII ratio. This combination provided a sensitivity of 84.6%, a specificity of 73.5%, a positive predictive value of 0.81%, and a negative predictive value of 99.6%.[11]
There may be some 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
elderly with atrophic gastritis or pernicious anemia, patients with partial
gastrectomy,[12] patients with the diagnosis of sporadic adenomas,[13]
familial adenomatous polyposis,[14] or hereditary nonpolyposis colon cancer,[15] and immigrant ethnic populations from countries with high
rates of gastric carcinoma.[16,17]
References
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Hisamuchi S, Fukao P, Sugawara N, et al.: Evaluation of mass screening programme for stomach cancer in Japan. In: Miller AB, Chamberlain J, Day NE, et al., eds.: Cancer Screening. Cambridge: Cambridge University Press, 1991, pp 357-372.
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Murakami R, Tsukuma H, Ubukata T, et al.: Estimation of validity of mass screening program for gastric cancer in Osaka, Japan. Cancer 65 (5): 1255-60, 1990.
[PUBMED Abstract]
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Kampschöer GH, Fujii A, Masuda Y: Gastric cancer detected by mass survey. Comparison between mass survey and outpatient detection. Scand J Gastroenterol 24 (7): 813-7, 1989.
[PUBMED Abstract]
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Oshima A, Hirata N, Ubukata T, et al.: Evaluation of a mass screening program for stomach cancer with a case-control study design. Int J Cancer 38 (6): 829-33, 1986.
[PUBMED Abstract]
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Hirayama T, Hisamichi S, Fujimoto I, et al.: Screening for gastric cancer. In: Miller AB, ed.: Screening for Cancer. New York, NY: Academic Press, 1985, pp 367-376.
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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. New York, NY: Raven Press, 1983, pp 305-318.
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Inaba S, Hirayama H, Nagata C, et al.: Evaluation of a screening program on reduction of gastric cancer mortality in Japan: preliminary results from a cohort study. Prev Med 29 (2): 102-6, 1999.
[PUBMED Abstract]
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Mizoue T, Yoshimura T, Tokui N, et al.: Prospective study of screening for stomach cancer in Japan. Int J Cancer 106 (1): 103-7, 2003.
[PUBMED Abstract]
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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.
[PUBMED Abstract]
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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.
[PUBMED Abstract]
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Kitahara F, Kobayashi K, Sato T, et al.: Accuracy of screening for gastric cancer using serum pepsinogen concentrations. Gut 44 (5): 693-7, 1999.
[PUBMED Abstract]
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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.
[PUBMED Abstract]
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Ming S, Goldman H: Gastric polyps: a histogenetic classification and its relation to carcinoma. Cancer 18(6): 721-726, 1965.
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Utsunomiya J, Maki T, Iwama T, et al.: Gastric lesion of familial polyposis coli. Cancer 34 (3): 745-54, 1974.
[PUBMED Abstract]
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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.
[PUBMED Abstract]
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Kurtz RC, Sherlock P: The diagnosis of gastric cancer. Semin Oncol 12 (1): 11-8, 1985.
[PUBMED Abstract]
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Boeing H: Epidemiological research in stomach cancer: progress over the last ten years. J Cancer Res Clin Oncol 117 (2): 133-43, 1991.
[PUBMED Abstract]
Back to Top Get More Information From NCI
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Back to Top Changes To This Summary (02/29/2008)
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.
Significance
Updated incidence and mortality estimates for 2008 (cited American Cancer Society as reference 1).
Back to Top Questions or Comments About This Summary
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