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Background  Methylation is a common epigenetic modification which may play a crucial role in cancer development. To investigate the association between methylation of  COX-2  in blood leukocyte DNA and risk of gastric cancer (GC), a nested case–control study was conducted in Linqu County, Shandong Province, a high risk area of GC in China.    Methods  Association between blood leukocyte DNA methylation of  COX-2  and risk of GC was investigated in 133 GCs and 285 superficial gastritis (SG)/ chronic atrophic gastritis (CAG). The temporal trend of  COX-2  methylation level during GC development was further explored in 74 pre-GC and 95 post-GC samples (including 31 cases with both pre- and post-GC samples). In addition, the association of DNA methylation and risk of progression to GC was evaluated in 74 pre-GC samples and their relevant intestinal metaplasia (IM)/dysplasia (DYS) controls. Methylation level was determined by quantitative methylation-specific PCR (QMSP). Odds ratios (ORs) and 95 % confidence intervals (CIs) were calculated by unconditional logistic regression analysis.    Results  The medians of  COX-2  methylation levels were 2.3 % and 2.2 % in GC cases and controls, respectively. No significant association was found between  COX-2  methylation and risk of GC (OR, 1.15; 95 % CI: 0.70-1.88). However, the temporal trend analysis showed that  COX-2  methylation levels were elevated at 1–4 years ahead of clinical GC diagnosis compared with the year of GC diagnosis (3.0 % vs. 2.2 %,  p  = 0.01). Further validation in 31 GCs with both pre- and post-GC samples indicated that  COX-2  methylation levels were significantly decreased at the year of GC diagnosis compared with pre-GC samples (1.5 %  vs.  2.5 %,  p  = 0.02). No significant association between  COX-2  methylation and risk of progression to GC was found in subjects with IM (OR, 0.50; 95 % CI: 0.18–1.42) or DYS (OR, 0.70; 95 % CI: 0.23–2.18). Additionally, we found that elder people had increased risk of  COX-2  hypermethylation (OR, 1.55; 95 % CI: 1.02–2.36) and subjects who ever infected with  H. pylori  had decreased risk of  COX-2  hypermethylation (OR, 0.54; 95 % CI: 0.34–0.88).    Conclusions   COX-2  methylation exists in blood leukocyte DNA but at a low level.  COX-2  methylation levels in blood leukocyte DNA may change during GC development.

Methylation status of COX-2 in blood leukocyte DNA and risk of gastric cancer in a high-risk Chinese population