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Eradication of Helicobacter pylori infection reverses E-cadherin promoter hypermethylation
  1. A O O Chan1,
  2. J Z Peng1,
  3. S K Lam1,
  4. K C Lai1,
  5. M F Yuen1,
  6. H K L Cheung1,
  7. Y L Kwong1,
  8. A Rashid2,
  9. C K Chan1,
  10. B C-Y Wong1
  1. 1Department of Medicine, University of Hong Kong, Hong Kong
  2. 2Department of Pathology, University of Texas, MD Anderson Cancer Center, Houston, Texas, USA
  1. Correspondence to:
    Dr B C-Y Wong
    Department of Medicine, University of Hong Kong, Queen Mary Hospital, Hong Kong; bcywong{at}hku.hk

Abstract

Background: E-cadherin methylation is important in gastric carcinogenesis. Reversing hypermethylation may halt the carcinogenic process. We have previously reported that Helicobacter pylori infection is associated with E-cadherin methylation in chronic gastritis patients.

Aim: To examine if eradication of H pylori could reverse E-cadherin methylation.

Methods: Patients with dyspepsia and positive for H pylori infection, with a mucosal biopsy showing chronic active gastritis, were randomised to receive H pylori eradication therapy (group 1, n = 41) or no treatment (group 2, n = 40), and were followed up prospectively. Gastric mucosae were taken for methylation assay at week 0 (before treatment) and week 6 (after treatment). Archived specimens of intestinal metaplasia with H pylori infection (n = 22) and without (n = 19) were retrieved for methylation analysis. Methylation was assessed using methylation specific polymerase chain reaction and sequencing.

Results: Methylation at E-cadherin was detected in 46% (19/41) and 17% (7/41) of patients at weeks 0 and 6, respectively, in group 1 (p = 0.004); 78.9% (15/19) of specimens were unmethylated after eradication of H pylori. Mucosal biopsy showed chronic inactive gastritis in 35 patients, intestinal metaplasia in one, and normal mucosa in five at week 6. Methylation was detected in 47.5% (19/40) and 52.5% (21/40) of patients at weeks 0 and 6, respectively, in group 2 (P = 0.5). Gastric mucosal biopsy showed persistent chronic active gastritis in all cases. Methylation frequency did not differ in H pylori positive or negative intestinal metaplastic specimens (72.7% v 63%; p = 0.5).

Conclusion:H pylori eradication therapy could reverse methylation in patients with chronic gastritis. This demonstrates an environmental effect on methylation.

  • PCR, polymerase chain reaction
  • MSP, methylation specific polymerase chain reaction
  • E-cadherin methylation
  • gastric cancer
  • intestinal metaplasia
  • Helicobacter pylori

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Footnotes

  • Conflict of interest: None declared.

  • The abstract was presented orally at the AGA Distinguished Abstract Plenary Session, GI Oncology Plenary Session: Frontiers of Clinical Medicine and Translational Research, Digestive Disease Week, New Orleans, USA, May 2004.

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