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Stomach (Gastric) Cancer Prevention (PDQ®)
Patient Version   Health Professional Version   Last Modified: 03/13/2008



Purpose of This PDQ Summary






Summary of Evidence






Significance






Evidence of Benefit






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Significance

Incidence and Mortality
Pathogenesis



Incidence and Mortality

The age-adjusted incidence rate in the United States for the years 2000 to 2003 was 8.1 per 100,000. Incidence among men is twice as high as among women.[1] Mortality rates for gastric cancer have been declining worldwide in recent decades, most prominently in the United States.[2,3] Mortality rates for white males in the United States were approximately 40 per 100,000 in 1930, compared with 5.8 per 100,000 for the years 1997 to 2001. The death rate from gastric cancer for black males was 2.3-fold higher than for whites for the years 1997 to 2001.[4] The annual number of new cases seems to be steady in recent years; in 2008, it is estimated 21,500 Americans will be diagnosed with gastric cancer and 10,880 will die of it.[5] Worldwide, gastric cancer is the fourth most common cancer.[6] Most cancers in the United States are advanced at diagnosis, which is reflected in an overall 5-year survival of 24.3% from 1996 to 2002.[1] 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.[7] In Japan, endoscopic resection techniques have been refined and may 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. (Refer to the PDQ summary on Stomach (Gastric) Cancer Screening for more information.)

Pathogenesis

Our understanding of the pathogenesis of gastric cancer has advanced in recent years. A prolonged 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 finally to invasive carcinoma.[8] 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. Ries LAG, Harkins D, Krapcho M, et al.: SEER Cancer Statistics Review, 1975-2003. Bethesda, Md: National Cancer Institute, 2006. Also available online. Last accessed October 07, 2008. 

  2. 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.  [PUBMED Abstract]

  3. Stomach. In: Ries LA, Kosary CL, Hankey BF, et al., eds.: SEER Cancer Statistics Review 1973-1995. Bethesda, Md: National Cancer Institute, 1998, Section 13. 

  4. American Cancer Society.: Cancer Facts and Figures 2005. Atlanta, Ga: American Cancer Society, 2005. Also available online. Last accessed July 31, 2008. 

  5. American Cancer Society.: Cancer Facts and Figures 2008. Atlanta, Ga: American Cancer Society, 2008. Also available online. Last accessed October 1, 2008. 

  6. Parkin DM: Global cancer statistics in the year 2000. Lancet Oncol 2 (9): 533-43, 2001.  [PUBMED Abstract]

  7. Tan YK, Fielding JW: Early diagnosis of early gastric cancer. Eur J Gastroenterol Hepatol 18 (8): 821-9, 2006.  [PUBMED Abstract]

  8. 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.  [PUBMED Abstract]

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