Abstract 157: Quantitative COX2 promoter methylation analysis in gastric carcinoma

• Published in: Cancer research (Chicago, Ill.) Ill.), 2010-04, Vol.70 (8_Supplement), p.157-157
• Main Authors: Bae, Woo-Kyun, Lee, Kyung-Hwa, Kim, Dong-Yi, Kim, Ho-Gun, Lee, Jae-Hyuk
• Format: Article
• Language: English
• ISSN: 0008-5472; 1538-7445
• DOI: 10.1158/1538-7445.AM10-157

Background: Epigenetic silencing of tumor-related genes, due to CpG island methylation, is considered to be an important mechanism for the development of many tumors, including gastric cancinoma. DNA methylation of multiple CpG sites in promoter regions of several tumor related genes, such as hMLH1, p14, p16, and APC has reported in gastric carcinoma. Recent studies indicate that aberrant CpG island methylation, and subsequent silencing of the COX-2 promoter, has been observed in a subset of gastric carcinomas (GC). To determine the occurrence of CpG island hypermethylation in GC in relation to H. pylori infection, the status and level of CpG methylation in promoter region of COX-2 was analyzed in early and advanced gastric carcinomas as opposed to normal gastric tissues. Materials and Methods: The extent of promoter methylation of COX-2 gene was assessed quantitatively using Pyrosequencing (PS) in 60 early gastric cancers (EGC) and 60 advanced gastric cancers (AGC) samples harvested upon gastrectomy, and 40 normal gastric mucosa samples from patients with benign gastric pathology. Giemsa stain was performed to detect H. pylori in neoplastic and non-neoplastic gastric mucosa. Gene product was studied by immunohistochemistry and the relationship between methylation profile of gene promoter and clinicopathological parameters was analyzed. Results: The PS analysis of GCs revealed a high frequency of COX-2 methylation in 30.0% (36/120). The methylation frequency for COX-2 gene by PS techniques was significantly higher in EGCs than in AGCs (40.0% and 20.0%, respectively, p