Data from Alterations of Cyclooxygenase-2 Methylation Levels Before and After Intervention Trial to Prevent Gastric Cancer in a Chinese Population

Abstract

<div>Abstract<p>To explore the epigenetic mechanisms underlying the effects of anti-<i>Helicobacter pylori</i> (<i>H. pylori</i>) alone and combined with COX-2 inhibitor (celecoxib), we dynamically evaluated the associations between <i>COX-2</i> methylation alterations and gastric lesion evolution during the process of interventions. In a total of 809 trial participants <i>COX-2</i> methylation levels were quantitatively detected before and after treatment. The self-comparison at the same stomach site for each subject showed significant methylation alteration differences among intervention groups (<i>P</i> < 0.001). With placebo group as reference, <i>COX-2</i> methylation levels were decreased in anti-<i>H. pylori</i> [OR, 3.30; 95% confidence interval (CI), 2.16–5.02], celecoxib (OR, 2.04; 95% CI, 1.36–3.07), and anti-<i>H. pylori</i> followed by celecoxib (OR, 2.10; 95% CI, 1.38–3.17) groups. When stratified by baseline histology, the three active arms significantly decreased <i>COX-2</i> methylation levels in indefinite dysplasia/dysplasia subjects, and ORs were 3.65 (95% CI, 1.96–6.80) for anti-<i>H. pylori</i>, 2.43 (95% CI 1.34–4.39) for celecoxib, and 2.80 (95% CI, 1.52–5.15) for anti-<i>H. pylori</i> followed by celecoxib, respectively. No additive effect on <i>COX-2</i> methylation was found for anti-<i>H. pylori</i> followed by celecoxib than two treatments alone. Compared with subjects without methylation reduction, higher opportunity for gastric lesion regression was found in subjects with decreased <i>COX-2</i> methylation levels, especially for indefinite dysplasia/dysplasia subjects (OR, 1.92; 95% CI, 1.03–3.60). These findings suggest that anti-<i>H. pylori</i> or celecoxib treatment alone could decrease <i>COX-2</i> methylation levels in gastric mucosa. <i>COX-2</i> methylation alteration was associated with the regression of indefinite dysplasia/dysplasia, which might serve as a potential biomarker for chemoprevention efficacy. <i>Cancer Prev Res; 9(6); 484–90. ©2016 AACR</i>.</p></div>