Journal
CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
Volume 4, Issue 1, Pages 47-53Publisher
ELSEVIER INC
DOI: 10.1016/j.jcmgh.2017.03.005
Keywords
Gastric Cancer; Inflammation; Cytokines
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Funding
- American Cancer Society Research Scholar Award [RSG-12-171-01-LIB]
- American Gastroenterological Association Institute Funderburg Award
- National Institutes of Health [RO1 DK110406-01]
- Arthritis National Research Foundation
- Saint Louis University Presidential Research Fund
- Washington University Digestive Disease Research Core Center seed grant
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Chronic inflammation caused by infection with Helicobacter pylori and autoimmune gastritis increases an individual's risk of developing gastric cancer. More than 90% of gastric cancers are adenocarcinomas, which originate from epithelial cells in the chronically inflamed gastric mucosa. However, only a small subset of chronic gastritis patients develops gastric cancer, implying a role for genetic and environmental factors in cancer development. A number of DNA polymorphisms that increase gastric cancer risk have mapped to genes encoding cytokines. Many different cytokines secreted by immune cells and epithelial cells during chronic gastritis have been identified, but a better understanding of how cytokines regulate the severity of gastritis, epithelial cell changes, and neoplastic transformation is needed. This review summarizes studies in both human and mouse models, describing a number of different findings that implicate various cytokines in regulating the development of gastric cancer.
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