DNA Methylation as Surrogate Marker For Gastric Cancer.
10.15430/JCP.2015.20.3.172
- Author:
Jung Hwan OH
1
;
Sung Hoon JUNG
;
Seung Jin HONG
;
Mun Gan RHYU
Author Information
1. Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.
- Publication Type:Review
- Keywords:
Biological markers;
CpG Islands;
DNA methylation;
Helicobacter pylori;
Stomach neoplasms
- MeSH:
Atrophy;
Biomarkers*;
CpG Islands;
Diagnosis;
DNA Methylation*;
DNA*;
Far East;
Gastric Mucosa;
Helicobacter pylori;
Humans;
Mass Screening;
Methylation;
Polymerase Chain Reaction;
Prognosis;
Recurrence;
Stomach Neoplasms*
- From:Journal of Cancer Prevention
2015;20(3):172-178
- CountryRepublic of Korea
- Language:English
-
Abstract:
Stomach cancer remains, stubbornly, highly prevalent in East Asia. Still, stomach cancer has few biomarkers by which it can be predicted. Helicobacter pylori infection, a known carcinogen of stomach cancer, usually goes undetected prior to cancer diagnosis, due to the poor mucosal environments that its related gastric atrophy causes. We propose, herein, an endoscopic-biopsy-based cancer-predicting DNA methylation marker. We semi-quantitatively examined the methylation-variable sites near the CpG-island margins by radioisotope-labeling methylation-specific polymerase chain reaction in association with H. pylori, which increases age-related over-methylation in CpG islands of gastric mucosa. These age-related methylation patterns of the transitional-CpG sites are proposed as useful surrogate markers for stomach cancer. It would be helpful for setting the optimal screening interval for high-risk subjects as well as for estimating the prognosis and the predictability for recurrence of early gastric cancer in patients having undergone endoscopic submucosal dissection. New screening-interval guidelines for gastric cancer should be suggested considering individual risk based on age, severity of atrophy, H. pylori status, and DNA methylation pattern.
