Effects of Helicobacter pylori infection on genetic instability, the aberrant CpG island methylation status and the cellular phenotype in Barrett's esophagus in a Japanese population
✍ Scribed by Kentaro Moriichi; Jiro Watari; Kiron M. Das; Hiroki Tanabe; Mikihiro Fujiya; Toshifumi Ashida; Yutaka Kohgo
- Publisher
- John Wiley and Sons
- Year
- 2009
- Tongue
- French
- Weight
- 289 KB
- Volume
- 124
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
Abstract
Genetic or epigenetic alterations in Barrett's esophagus (BE) with/without Helicobacter pylori (H. pylori) infection remain unclear. We examined the effects of H. pylori infection on genetic instability (GIN), the CpG island methylation status and a biomarker related to BE carcinogenesis. We analyzed 113 Japanese individuals with endoscopically suspected BE. The patients included, Group CLE (n = 25): no specialized intestinal metaplasia (SIM) in a columnar lined epithelium (control); Group BE (n = 88): all had SIM. Microsatellite instability and a loss of heterozygosity as GIN, the methylation status at hMLH1, E‐cadherin, p16 and APC, and immunoreactivity using a monoclonal antibody (mAb) Das‐1, which specifically reacts with BE, were evaluated. Nine additional patients with BE were prospectively followed up for 2 years after successful H. pylori eradication. The frequency of GIN, methylation at E‐cadherin and APC, and mAb Das‐1 reactivity in Group BE was significantly higher than that in Group CLE (p < 0.0001, p < 0.0001 and p < 0.005, and p < 0.0001, respectively). Furthermore, GIN, E‐cadherin methylation and mAb Das‐1 reactivity showed a significantly higher incidence in patients with H.pylori infection than in those without H. pylori infection (p < 0.01, p < 0.005, and p < 0.01, respectively). Interestingly, the patients from Group BE were observed to change to a stable state of molecular alterations in 60% for GIN, 42.9% for E‐cadherin methylation and 55.6% for APC methylation, or a reduction of mAb Das‐1 reactivity was noted in 25% following eradication. H. pylori infection may therefore affect these molecular alterations associated with the pathogenesis of BE, to some degree, in the Japanese population. © 2008 Wiley‐Liss, Inc.