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    Stomach (Gastric) Cancer Prevention (PDQ®): Prevention - Health Professional Information [NCI] - Description of the Evidence



    Understanding 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.[9] 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 H. pylori.

    Interventions for Reduction of Stomach (Gastric) Cancer Risk

    Smoking cessation

    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.[10] A systematic review of studies addressing the relationship between cigarette smoking and gastric cancer to estimate the magnitude of the association for different levels of exposure to cancer provides solid evidence to classify smoking as the most important behavioral risk factor for gastric cancer.[10,11,12] Compared with persistent smokers, the risk of stomach cancer decreases among former 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

    H. pylori infection is an accepted cause of gastric adenocarcinoma.[13,14] Questions remain concerning the natural history of H. pylori infection; the mechanism of transmission and the rates of reinfection or recrudescence for different populations are unknown.[15,16] A small randomized trial of antibiotic eradication in 140 H. pylori-infected people suggests the possibility of transmission among close family members.[17] 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.

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