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Updated: May 27, 2026

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
Published on: September 18, 2020
Alterations in cell proliferation related gene expressions in gastric cancer
Kyungtae Kim1, Kyung-Hee Chun, Pann-Ghill Suh
1Research Institute, National Cancer Center, Gyeonggido, Republic of Korea.
Abstract:
Gastric cancer remains the fourth most prevalent cancer and the second leading cause of cancer-related death in the world. The predominant form of gastric cancer is adenocarcinoma, which originates from glandular epithelium of the gastric mucosa. The major risk factors for gastric cancer include diet, individual genetic variation, and, most importantly, infection with Helicobacter pylori (H. pylori). Certain strains of H. pylori assisted by some of its virulence factors seem to play a critical role in gastric cancer development. Several of these H. pylori virulence factors, which influence cellular proliferation signaling, have been identified. In addition, changes in the expression of several cell proliferation regulating genes accompany or cause the progression of gastric cancer. These changes include modifications of cell cycle regulators, oncogene activation, tumor suppressor inactivation, and miRNA profile alterations. Many of these changes result from H. pylori infection, although their impact on the cellular proliferation system underlying gastric cancer development has not yet been fully elucidated. We review certain features of gastric cancer, the role of H. pylori infection in its etiology and pathogenesis, and gene expression changes during gastric carcinogenesis.
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