A comparative study of CDO1 promoter methylation in gastric cancer and H. pylori-associated chronic gastritis: Implications for diagnostic performance
PloS one, cilt.21, sa.8, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 21 Sayı: 8
- Basım Tarihi: 2026
- Doi Numarası: 10.1371/journal.pone.0335832
- Dergi Adı: PloS one
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, L'Année philologique, Aerospace Database, BIOSIS, Chemical Abstracts Core, EMBASE, Index Islamicus, Linguistic Bibliography, MEDLINE, Psycinfo, zbMATH, Directory of Open Access Journals, Zoological Record, Academic Search Ultimate (EBSCO), Natural Science Collection (ProQuest), Biological Science Database (ProQuest), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest), Materials Science & Engineering Collection (ProQuest), Pharma Collection (ProQuest), Technology Collection (ProQuest)
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- İstanbul Yeni Yüzyıl Üniversitesi Adresli: Evet
Özet
Silencing of the Cysteine dioxygenase-1 (CDO1) tumor suppressor gene by aberrant DNA methylation contributes to gastric carcinogenesis. Despite evidence that Helicobacter pylori (H. pylori) infection induces aberrant DNA methylation in the gastric mucosa, CDO1 promoter methylation has not been well characterized in H. Pylori positive (HPP) patients with chronic gastritis. This study aimed to investigate the CDO1 promoter methylation levels in patients with chronic gastritis with and without H. pylori infection, in comparison with gastric tumors. The quantitative analysis of CDO1 promoter methylation and CDO1 immunopositivity was performed in 45 primary gastric tumors, 17 biopsy samples of HPP chronic gastritis, 23 H. Pylori negative (HPN) chronic gastritis, and 15 normal gastric mucosa samples (control group). CDO1 expression was evaluated by immunohistochemistry, and promoter methylation levels were determined using quantitative methylation-specific PCR following bisulfite conversion. CDO1 promoter methylation levels were significantly higher in the gastric cancer (GC) group compared to the HPN chronic gastritis and control groups (p < 0.001). No significant difference was observed between the GC and HPP chronic gastritis groups. However, CDO1 promoter methylation levels were significantly higher in the HPP group compared to the HPN group (p = 0.049). No significant differences in CDO1 immunopositivity were observed among the study groups. ROC analysis demonstrated good discriminative ability of CDO1 methylation between GC and non-cancer cases (AUC = 0.83), whereas its performance was more limited in distinguishing GC from HPP chronic gastritis (AUC = 0.67). CDO1 promoter methylation is increased in GC and HPP chronic gastritis, suggesting that H. pylori-associated chronic inflammation may be associated with early epigenetic alterations. Although no direct correlation with protein expression was observed, our findings suggest that while CDO1 methylation may be informative for identifying cancer-related epigenetic changes, it may be insufficient as a standalone biomarker in high-risk inflammatory conditions. Further studies are needed to clarify its clinical utility, particularly in high-risk populations.