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      Gastric Cancer: How Can We Reduce the Incidence of this Disease?

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          Abstract

          Gastric cancer remains a prevalent disease worldwide with a poor prognosis. Helicobacter pylori plays a major role in gastric carcinogenesis. H. pylori colonization leads to chronic gastritis, which predisposes to atrophic gastritis, intestinal metaplasia, dysplasia, and eventually gastric cancer. Screening, treatment, and prevention of H. pylori colonization can reduce the incidence of gastric cancer. Other interventions that may yield a similar effect, although of smaller magnitude, include promotion of a healthy lifestyle including dietary measures, non-smoking, low alcohol intake, and sufficient physical activity. This chapter reviews interventions that can lead to a decline in gastric cancer incidence in high and low incidence countries.

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          Most cited references44

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          Effect of eradication of Helicobacter pylori on incidence of metachronous gastric carcinoma after endoscopic resection of early gastric cancer: an open-label, randomised controlled trial.

          The relation between Helicobacter pylori infection and gastric cancer has been proven in epidemiological studies and animal experiments. Our aim was to investigate the prophylactic effect of H pylori eradication on the development of metachronous gastric carcinoma after endoscopic resection for early gastric cancer. In this multi-centre, open-label, randomised controlled trial, 544 patients with early gastric cancer, either newly diagnosed and planning to have endoscopic treatment or in post-resection follow-up after endoscopic treatment, were randomly assigned to receive an H pylori eradication regimen (n=272) or control (n=272). Randomisation was done by a computer-generated randomisation list and was stratified by whether the patient was newly diagnosed or post-resection. Patients in the eradication group received lansoprazole 30 mg twice daily, amoxicillin 750 mg twice daily, and clarithromycin 200 mg twice daily for a week; those in the control group received standard care, but no treatment for H pylori. Patients were examined endoscopically at 6, 12, 24, and 36 months after allocation. The primary endpoint was diagnosis of new carcinoma at another site in the stomach. Analyses were by intention to treat. This trial is registered with the UMIN Clinical Trials Registry, number UMIN000001169. At 3-year follow-up, metachronous gastric carcinoma had developed in nine patients in the eradication group and 24 in the control group. In the full intention-to-treat population, including all patients irrespective of length of follow-up (272 patients in each group), the odds ratio for metachronous gastric carcinoma was 0.353 (95% CI 0.161-0.775; p=0.009); in the modified intention-to-treat population, including patients with at least one post-randomisation assessment of tumour status and adjusting for loss to follow-up (255 patients in the eradication group, 250 in the control group), the hazard ratio for metachronous gastric carcinoma was 0.339 (95% CI 0.157-0.729; p=0.003). In the eradication group, 19 (7%) patients had diarrhoea and 32 (12%) had soft stools. Prophylactic eradication of H pylori after endoscopic resection of early gastric cancer should be used to prevent the development of metachronous gastric carcinoma. Hiroshima Cancer Seminar Foundation.
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            Fifteen-year effects of Helicobacter pylori, garlic, and vitamin treatments on gastric cancer incidence and mortality.

            In the Shandong Intervention Trial, 2 weeks of antibiotic treatment for Helicobacter pylori reduced the prevalence of precancerous gastric lesions, whereas 7.3 years of oral supplementation with garlic extract and oil (garlic treatment) or vitamin C, vitamin E, and selenium (vitamin treatment) did not. Here we report 14.7-year follow-up for gastric cancer incidence and cause-specific mortality among 3365 randomly assigned subjects in this masked factorial placebo-controlled trial. Conditional logistic regression was used to estimate the odds of gastric cancer incidence, and the Cox proportional hazards model was used to estimate the relative hazard of cause-specific mortality. All statistical tests were two-sided. Gastric cancer was diagnosed in 3.0% of subjects who received H pylori treatment and in 4.6% of those who received placebo (odds ratio = 0.61, 95% confidence interval = 0.38 to 0.96, P = .032). Gastric cancer deaths occurred among 1.5% of subjects assigned H pylori treatment and among 2.1% of those assigned placebo (hazard ratio [HR] of death = 0.67, 95% CI = 0.36 to 1.28). Garlic and vitamin treatments were associated with non-statistically significant reductions in gastric cancer incidence and mortality. Vitamin treatment was associated with statistically significantly fewer deaths from gastric or esophageal cancer, a secondary endpoint (HR = 0.51, 95% CI = 0.30 to 0.87; P = .014).
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              A model for gastric cancer epidemiology.

              It is postulated that one major subtype of gastric carcinoma ("intestinal type") is the end- result of a series of mutations and cell transformation begun in the first decade of life. The mutagen could be a nitroso compound synthesised in the upper gastrointestinal tract by the action of nitrite (i.e., from food or saliva) on naturally occurring nitrogen compounds. Under normal conditions these nitroso compounds do not reach the gastric epithelial cell, presumably because their synthesis is inhibited by antioxidants present in food or because of their inability to pass the mucous barrier. The barrier may be overcome by abrasives or irritants such as hard grains, food with high sodium-chloride concentration, or surfactants. Once the first mutation occurs, the glandular gastric epithelium is gradually changed to intestinal-type epithelium, the mucous barrier altered, and the pH elevated. Under these conditions, bacteria proliferate in the gastric cavity and facilitate the conversion of nitrates to nitrites, thereby increasing the nitrite pool and the probability of formation of mutagenic-carcinogenic nitroso compounds. This process of gastric atrophy and intestinal metaplasia goes on for 30 to 50 years until some of the individuals affected have the final mutation or cell transformation which allows the cell to become autonomous and invade other tissues.
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                Author and article information

                Contributors
                c.denhoed@erasmusmc.nl
                Journal
                Curr Gastroenterol Rep
                Curr Gastroenterol Rep
                Current Gastroenterology Reports
                Springer US (New York )
                1522-8037
                1534-312X
                16 May 2016
                16 May 2016
                2016
                : 18
                Affiliations
                Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands
                Article
                506
                10.1007/s11894-016-0506-0
                4868864
                27184043
                7ba9fb0c-7811-4a56-ba14-7d84788a9ed1
                © The Author(s) 2016

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                Categories
                GI Oncology (R Bresalier, Section Editor)
                Custom metadata
                © Springer Science+Business Media New York 2016

                Gastroenterology & Hepatology
                gastric cancer,epidemiology,prevention,helicobacter pylori,diet,screening

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