Pathogenesis and risk factors for gastric cancer after Helicobacter pylori eradication

doi:10.4251/wjgo.v8.i9.663

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Sep 15, 2016 (publication date) through Apr 26, 2024

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World Journal of Gastrointestinal Oncology

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1948-5204

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Gastrointest Oncol. Sep 15, 2016; 8(9): 663-672
Published online Sep 15, 2016. doi: 10.4251/wjgo.v8.i9.663

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Figure 1 Relationship between gastric mucosae methylation levels and Helicobacter pylori infection/gastric cancer (modified from Maekita et al[22]). Residual aberrant methylation even after eradication is thought to reflect methylation in gastric gland stem cells. From endoscopically biopsied tissue, predicting GC risk based on the accumulation of aberrant DNA methylation in the gastric mucosae. ESD: Endoscopic submucosal resection; GC: Gastric cancer; H. pylori: Helicobacter pylori.

Citation: Ohba R, Iijima K. Pathogenesis and risk factors for gastric cancer after Helicobacter pylori eradication. World J Gastrointest Oncol 2016; 8(9): 663-672
URL: https://www.wjgnet.com/1948-5204/full/v8/i9/663.htm
DOI: https://dx.doi.org/10.4251/wjgo.v8.i9.663