| Theme | Gastric Cancer Screening -- Present Status and Uprising High-risk Strategy | |
|---|---|---|
| Title | Possibility of Epigenetic Markers for Gastric Cancer Risk Diagnosis | |
| Publish Date | 2008/03 | |
| Author | Shotaro Enomoto | Carcinogenesis Division, National Cancer Center Research Institute / Second Department of Internal Medicine, Wakayama Medical University |
| Author | Takayuki Ando | Carcinogenesis Division, National Cancer Center Research Institute |
| Author | Toshikazu Ushijima | Carcinogenesis Division, National Cancer Center Research Institute |
| [ Summary ] | Epigenetic alterations, represented by aberrant DNA methylation, are deeply involved in gastric carcinogenesis, in addition to genetic alterations. It was recently shown that H. pylori infection, a potent gastric carcinogenic factor, induces DNA methylation of specific genes in the gastric mucosae, and that DNA methylation levels of specific genes in the gastric mucosae correlate with risk of gastric cancer in individuals without current H. pylori infection. The gastric mucosa without clonal lesions however is predisposed to cancer development, designated as a “field for cancerization” or “field defect”. This seems to be induced by H. pylori infection, and its degree can be measured using DNA methylation levels for appropriate marker genes. It is expected that aberrant DNA methylation in the gastric mucosae is useful as a risk marker for gastric cancer. | |