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Gut Microbes. 2013 Nov-Dec;4(6):482-93. doi: 10.4161/gmic.26262. Epub 2013 Sep 3.

Diet, microbial virulence, and Helicobacter pylori-induced gastric cancer.

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Division of Infectious Diseases; Vanderbilt University School of Medicine; Nashville, TN USA; Department of Pathology, Microbiology, and Immunology; Vanderbilt University School of Medicine; Nashville, TN USA; Veterans Affairs Tennessee Valley Healthcare System; Nashville, TN USA.
Division of Gastroenterology, Department of Medicine; Vanderbilt University School of Medicine; Nashville, TN USA.


Gastric adenocarcinoma is a leading cause of cancer-related death worldwide, and Helicobacter pylori infection is one of the strongest known risk factors for this malignancy. H. pylori strains exhibit a high level of genetic diversity, and the risk of gastric cancer is higher in persons carrying certain strain types (for example, those that contain a cag pathogenicity island or type s1 vacA alleles) than in persons carrying other strain types. Additional risk factors for gastric cancer include specific human genetic polymorphisms and specific dietary preferences (for example, a high-salt diet or a diet deficient in fruits and vegetables). Finally, iron-deficiency anemia is a risk factor for gastric cancer. Recent studies have provided evidence that several dietary risk factors for gastric cancer directly impact H. pylori virulence. In this review article, we discuss mechanisms by which diet can modulate H. pylori virulence and thereby influence gastric cancer risk.


BabA; CagA; VacA; cagpathogenicity island; diet; gastric adenocarcinoma; gastric cancer; iron; salt

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