title: Helicobacter pylori eradication prevents extension of intestinalization even in the high-risk group for gastric cancer.
abstract: OBJECTIVE
  CDX2 is associated with the intestinal phenotype in the gastrointestinal tracts and is expressed in the intestinal type of gastric cancer. Helicobacter pylori-associated atrophic gastritis is characterized by aberrant expression of CDX2. The aim was to investigate the effects of eradication to the expression of genes related to the gastric and intestinal phenotype including CDX2. We compared the effect of eradication between the patients at high risk for gastric cancer and controls.
  
  
  METHODS
  20 patients with endoscopic resection for early gastric cancer and 12 sex- and age-matched controls were studied. CDX2 and mucin mRNA expressions were examined using whole biopsy specimens and microdissected gastric glands taken from corpus lesser and greater curves before and 1 year after eradication.
  
  
  RESULTS
  CDX2 and MUC2 expressions in the cancer group were significantly higher than in the controls and were significantly decreased after eradication. MUC5AC (p = 0.01) and MUC6 (p = 0.02) expression significantly increased in the control group; the difference between the two groups became significant after eradication. CDX2 expression in the glands without goblet cells was detectable and disappeared after eradication.
  
  
  CONCLUSIONS
  H. pylori eradication can reverse gastric phenotype and diminish aberrant CDX2 expression in the early stage of intestinalization.
authors.affiliation: Division of Gastroenterology, Department of Internal Medicine, Kawasaki Medical School, Kurashiki, Japan. shiotani@med.kawasaki-m.ac.jp
authors.forename: Akiko
authors.initials: A
authors.lastname: Shiotani
authors.forename: Ryuji
authors.initials: R
authors.lastname: Nishi
authors.forename: Noriya
authors.initials: N
authors.lastname: Uedo
authors.forename: Hiroyasu
authors.initials: H
authors.lastname: Iishi
authors.forename: Hideaki
authors.initials: H
authors.lastname: Tsutsui
authors.forename: Manabu
authors.initials: M
authors.lastname: Ishii
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Imamura
authors.forename: Tomoari
authors.initials: T
authors.lastname: Kamada
authors.forename: Jiro
authors.initials: J
authors.lastname: Hata
authors.forename: Ken
authors.initials: K
authors.lastname: Haruma
mesh_terms: D000368:Aged; D000900:Anti-Bacterial Agents / Q000008:administration & dosage; D001707:Biopsy, Needle; D000071616:CDX2 Transcription Factor; D016022:Case-Control Studies; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology / Q000601:surgery; D005773:Gastroscopy / Q000379:methods; D016481:Helicobacter Infections / Q000150:complications / Q000188:drug therapy* / Q000473:pathology; D016480:Helicobacter pylori / Q000187:drug effects* / Q000302:isolation & purification; D018398:Homeodomain Proteins / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D011230:Precancerous Conditions / Q000235:genetics / Q000473:pathology; D011336:Probability; D054328:Proton Pump Inhibitors / Q000008:administration & dosage; D012333:RNA, Messenger / Q000032:analysis; D012016:Reference Values; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018570:Risk Assessment; D018709:Statistics, Nonparametric; D013274:Stomach Neoplasms / Q000473:pathology / Q000517:prevention & control* / Q000601:surgery; D015534:Trans-Activators / Q000235:genetics / Q000378:metabolism*; D016896:Treatment Outcome
chemical_list: D000900:Anti-Bacterial Agents; D000071616:CDX2 Transcription Factor; D018398:Homeodomain Proteins; D054328:Proton Pump Inhibitors; D012333:RNA, Messenger; D015534:Trans-Activators