Print

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

Issue: Vol.11, No.1 - January 2012

« Back to Articles

Article Type: Manuscript

Download PDF Version »

  1. Dr Jiro Watari
    Division of Upper Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine,
  2. Dr Kentaro Morichi
    Division of Gastroenterology and Hematology/Oncology, Department of Medicine, Asahikawa Medical University, ,
  3. Dr Kiron M. Das
    Crohn’s and Colitis Centre of New Jersey, Division of Gastroenterology and Hepatology, UMDNJ-Robert Wood Johnson Medical Schoolrn
  4. Dr Hiroki Tanabe
    Division of Gastroenterology and Hematology/Oncology, Department of Medicine, Asahikawa Medical University, ,
  5. Dr Mikihiro Fujiya
    Division of Gastroenterology and Hematology/Oncology, Department of Medicine, Asahikawa Medical University,
  6. Toshifumi Ashida
    Division of Gastroenterology and Hematology/Oncology, Department of Medicine, Asahikawa Medical University, ,
  7. Dr Yutaka Kohgo
    Division of Gastroenterology and Hematology/Oncology, Department of Medicine, Asahikawa Medical University, ,

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 yrs 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.

 

Download PDF Version »

Favourites   Share / Bookmark

Also In This Issue

« Back to Articles