Gastric cancer: Screening - Health Professional Information [NCI PDQ]

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Gastric Cancer Screening (PDQ®)

Summary of Evidence

Note: Separate PDQ summaries on Prevention of Gastric Cancer, 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

• STUDY DESIGN: Evidence obtained from case-control studies.
• INTERNAL VALIDITY: Fair.
• CONSISTENCY: Multiple studies, large number of participants.
• MAGNITUDE OF EFFECTS ON HEALTH OUTCOMES: Fair evidence for no reduction in mortality.
• 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

• STUDY DESIGN: Evidence obtained from well-designed and conducted case-control studies.
• INTERNAL VALIDITY: Fair.
• CONSISTENCY: Multiple studies, large number of participants.
• MAGNITUDE OF EFFECTS ON HEALTH OUTCOMES: Good evidence for rare but serious harms.

Significance

Natural History, Incidence, and Mortality

Gastric cancer is the 14th most frequent cause of cancer mortality in the United States. In 2007, it is estimated that 21,260 Americans will be diagnosed with gastric cancer and 11,210 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. In fact, it 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. These 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 7 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.[6,7,8] 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:

1. American Cancer Society.: Cancer Facts and Figures 2007. Atlanta, Ga: American Cancer Society, 2007. Also available online. Last accessed September 7, 2007.
2. American Cancer Society.: Cancer Facts and Figures 2005. Atlanta, Ga: American Cancer Society, 2005. Also available online. Last accessed February 9, 2007.
3. 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.
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. Crew KD, Neugut AI: Epidemiology of gastric cancer. World J Gastroenterol 12 (3): 354-62, 2006.
6. Parsonnet J, Hansen S, Rodriguez L, et al.: Helicobacter pylori infection and gastric lymphoma. N Engl J Med 330 (18): 1267-71, 1994.
7. 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.
8. 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.
9. 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.
10. 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.
11. Greene FL: Neoplastic changes in the stomach after gastrectomy. Surg Gynecol Obstet 171 (6): 477-80, 1990.

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 2-fold decrease in gastric cancer mortality in screened versus unscreened individuals.[2,3,4,5,6] 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:

1. 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.
2. 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.
3. 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.
4. 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.
5. 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.
6. 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.
7. 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.
8. 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.
9. 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.
10. 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.
11. Kitahara F, Kobayashi K, Sato T, et al.: Accuracy of screening for gastric cancer using serum pepsinogen concentrations. Gut 44 (5): 693-7, 1999.
12. 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.
13. Ming S, Goldman H: Gastric polyps: a histogenetic classification and its relation to carcinoma. Cancer 18(6): 721-726, 1965.
14. Utsunomiya J, Maki T, Iwama T, et al.: Gastric lesion of familial polyposis coli. Cancer 34 (3): 745-54, 1974.
15. 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.
16. Kurtz RC, Sherlock P: The diagnosis of gastric cancer. Semin Oncol 12 (1): 11-8, 1985.
17. Boeing H: Epidemiological research in stomach cancer: progress over the last ten years. J Cancer Res Clin Oncol 117 (2): 133-43, 1991.

Changes To This Summary (03/05/2007)

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 2007 (cited American Cancer Society as reference 1).

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Date Last Modified: 2007-03-05

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