Background Epigenetic alteration through promoter DNA methylation is associated with gastric carcinogenesis. This study assessed the association between Helicobacter pylori infection, specifically cagA -positive strains, and MGMT promoter hypermethylation within the gastroduodenal disease spectrum in an Iraqi cohort. Methods The study conducted a case control study of 120 participants (40 endoscopy confirmed controls without gastroduodenal disease and 80 patients with gastritis, peptic ulcer disease, lymphoma, or gastric adenocarcinoma). Standard OGD biopsies were collected. H. pylori status was determined by rapid urease testing, selective culture on blood agar with biochemical identification, and PCR confirmation; cagA was detected by conventional PCR using validated primers and cycling conditions. Genomic DNA was separated and bisulfite treatment converted. MGMT promoter methylation was measured by methylation specific PCR primers and bisulfate treatment. Statistical analyses used chi-square or chi-square and reported odds ratios with 95% confidence intervals. Results The results showed a significantly greater incidence of H. pylori than controls (72.5% vs. 0%; χ 2 =56.129, pCagA was found in 56.3% of patients and 0% of controls (χ 2 =36.000, pMGMT promoter hypermethylation was observed in 66.3% of patients, whereas none of the controls exhibited this condition (χ 2 =47.463, p2 (15)=66.433, p, H. pylori positivity exhibited a significant correlation with hypermethylation (43/58 vs 10/62; χ 2 =40.892, pcagA positivity demonstrated an even more pronounced association (41/45 vs 12/75; χ 2 =64.345, p2 (2)=15.218, p0.10). Conclusions MGMT promoter hypermethylation is prevalent in gastroduodenal diseases in Iraqi cases, with H. pylori infection strongly correlated with MGMT hypermethylation, suggesting MGMT methylation as a biomarker for risk stratification.
Ahmed et al. (Tue,) studied this question.