title: Severity of atrophic gastritis related to antiparietal cell antibody and gastric carcinogenesis, including p53 mutations.
abstract: OBJECTIVE
  Infection with Helicobacter pylori (Hp) has been linked to atrophic gastritis, an inflammatory precursor of non-cardia gastric carcinoma. Mutations in the p53 gene are one of the most frequent genetic alterations in gastric carcinoma. In a subgroup of atrophic gastritis, antiparietal cell antibody (APCA) has been detected. This study was aimed to clarify the role of APCA in the progression of atrophic gastritis and gastric carcinogenesis, and to determine the relationship of the severity of atrophic gastritis to gastric carcinoma and to p53 mutations.
  
  
  METHODS
  In 494 control subjects and 284 gastric carcinoma patients, serum APCA was evaluated and all subjects and patients were classified into four groups using serologic markers (anti-Hp IgG antibody and pepsinogen (PG) test: positive; PG I < 70 microg/L and PG I/II ratio < 3.0) as follows: A, HP- PG-; B, HP+ PG-; C, HP+ PG+ and D, HP- PG+. p53 mutations were analyzed in 174 of 284 patients.
  
  
  RESULTS
  Antiparietal cell antibody seropositivity increased from group B to D, however, no difference in its positivity was found between controls and patients. The incidence of gastric carcinoma increased from A to D, especially the intestinal subtype. The frequency of p53 gene mutations was higher in PG+ than in PG- gastric carcinoma.
  
  
  CONCLUSIONS
  Antiparietal cell antibody seropositivity is involved in the progression of a subgroup of atrophic gastritis, but not associated with gastric carcinogenesis. Severe atrophic gastritis is associated with susceptibility to gastric carcinoma, especially the intestinal subtype, and p53 mutations.
authors.affiliation: Division of Gastroenterology, Department of Therapeutic Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan.
authors.forename: Ayumu
authors.initials: A
authors.lastname: Taguchi
authors.forename: Naoki
authors.initials: N
authors.lastname: Ohmiya
authors.forename: Akihiro
authors.initials: A
authors.lastname: Itoh
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Hirooka
authors.forename: Yasumasa
authors.initials: Y
authors.lastname: Niwa
authors.forename: Naoyoshi
authors.initials: N
authors.lastname: Mori
authors.forename: Hidemi
authors.initials: H
authors.lastname: Goto
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000888:Antibodies, Anti-Idiotypic / Q000032:analysis*; D016009:Chi-Square Distribution; D018450:Disease Progression; D005260:Female; D005757:Gastritis, Atrophic / Q000145:classification / Q000235:genetics* / Q000276:immunology* / Q000382:microbiology; D016481:Helicobacter Infections / Q000150:complications / Q000276:immunology; D016480:Helicobacter pylori / Q000276:immunology; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009154:Mutation; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric; D013274:Stomach Neoplasms / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
chemical_list: D000888:Antibodies, Anti-Idiotypic; D016159:Tumor Suppressor Protein p53