title: H. pylori eradication did not improve dysregulation of specific oncogenic miRNAs in intestinal metaplastic glands.
abstract: BACKGROUND
  Many microRNAs (miRNAs) are differentially expressed in Helicobacter pylori-infected gastric mucosa and in gastric cancer tissue.
  
  
  OBJECTIVE
  We aimed to compare the effect of H. pylori eradication on gastric mucosal miRNAs in subjects in a high-risk group for gastric cancer compared to controls.
  
  
  METHODS
  Patients with a recent history of endoscopic resection for early gastric cancer and sex- and age-matched non-cancer controls were enrolled. The expression of 21 miRNAs was examined using gastric mucosal biopsy specimens and microdissected gastric glands from the lesser and greater curvatures of the gastric corpus both before and one year after H. pylori eradication.
  
  
  RESULTS
  Twenty patients and 14 controls were enrolled. The expression of oncogenic miRNAs (miR-17/92 and the miR-106b-93-25 cluster, miR-21, miR-194, and miR-196) was significantly higher in the gastric mucosa of the cancer group than in the controls. H. pylori eradication resulted in a significant fall in the expression of oncogenic miRNAs only in the controls, whereas miR-223 expression was decreased and let-7d expression was increased in both groups. miR-196 was expressed only in intestinal metaplastic glands. The expression of oncogenic miRNAs was significantly higher in the intestinal metaplastic glands than in the non-intestinal metaplastic glands irrespective of H. pylori eradication. In neither group did H. pylori eradication significantly change any miRNA expression in the intestinal metaplastic glands.
  
  
  CONCLUSIONS
  Dysregulation of specific miRNAs is present in H. pylori-induced corpus gastritis. H. pylori eradication improved miRNA dysregulation, but not in intestinal metaplastic glands or in the gastric mucosa of patients in a high-risk group for gastric cancer.
authors.affiliation: Division of Gastroenterology, Department of Internal Medicine, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japan. shiotani@med.kawasaki-m.ac.jp
authors.forename: Akiko
authors.initials: A
authors.lastname: Shiotani
authors.forename: Noriya
authors.initials: N
authors.lastname: Uedo
authors.forename: Hiroyasu
authors.initials: H
authors.lastname: Iishi
authors.forename: Takahisa
authors.initials: T
authors.lastname: Murao
authors.forename: Tomoko
authors.initials: T
authors.lastname: Kanzaki
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Kimura
authors.forename: Tomoari
authors.initials: T
authors.lastname: Kamada
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Kusunoki
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Inoue
authors.forename: Ken
authors.initials: K
authors.lastname: Haruma
mesh_terms: D000368:Aged; D000658:Amoxicillin / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D001706:Biopsy; D016022:Case-Control Studies; D017291:Clarithromycin / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism; D005773:Gastroscopy; D005786:Gene Expression Regulation / Q000502:physiology*; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000235:genetics / Q000382:microbiology; D016480:Helicobacter pylori / Q000472:pathogenicity; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008679:Metaplasia / Q000473:pathology; D035683:MicroRNAs / Q000235:genetics*; D008875:Middle Aged; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D054328:Proton Pump Inhibitors / Q000627:therapeutic use; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013274:Stomach Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000382:microbiology
chemical_list: D000900:Anti-Bacterial Agents; D035683:MicroRNAs; D011518:Proto-Oncogene Proteins; D054328:Proton Pump Inhibitors; D000658:Amoxicillin; D017291:Clarithromycin