title: Helicobacter pylori and the null genotype of glutathione-S-transferase-mu in patients with gastric adenocarcinoma.
abstract: BACKGROUND
  Chronic Helicobacter pylori infection now is recognized as an important causative agent for gastric carcinoma. However, only a small minority of infected individuals develop the malignancy, even in areas with a high prevalence of gastric carcinoma. It has been postulated that the absence of glutathione-S-transferase-mu (GST-mu), which impairs detoxification of exogenous carcinogens, might predispose some infected individuals to the development of gastric carcinoma.
  
  
  METHODS
  Patients with histologically confirmed adenocarcinoma of the stomach were tested for H. pylori infection and the GST-mu genotype. Prevalence of GST-mu gene deletion was compared with the H. pylori status of the patients. A group of gender- and age-matched control subjects with known H. pylori-related nonulcer dyspepsia also were tested for the GST-mu genotype and compared with patients with H. pylori positive carcinoma.
  
  
  RESULTS
  Fifty-one patients with gastric adenocarcinoma were enrolled into the study. Thirty-five were found to have H. pylori in the resected specimens. The null genotype of GST-mu was significantly more common among those patients with H. pylori positive carcinoma compared with the H. pylori negative group (65.7% vs. 31.3%; P < 0.05). Homozygous deletion of GST-mu was significantly higher in the H. pylori positive carcinoma patients than in the H. pylori-infected, nonmalignant control group (65.7% vs. 37.1%; P < 0.05).
  
  
  CONCLUSIONS
  The null genotype for GST-mu is found more commonly in gastric carcinoma associated with H. pylori infection. The absence of the GST-mu enzyme may increase the risk of the development of gastric carcinoma in these patients.
authors.affiliation: Department of Surgery, Prince of Wales Hospital, Shatin, N.T., Hong Kong.
authors.forename: E K
authors.initials: EK
authors.lastname: Ng
authors.forename: J J
authors.initials: JJ
authors.lastname: Sung
authors.forename: T K
authors.initials: TK
authors.lastname: Ling
authors.forename: S M
authors.initials: SM
authors.lastname: Ip
authors.forename: J Y
authors.initials: JY
authors.lastname: Lau
authors.forename: A C
authors.initials: AC
authors.lastname: Chan
authors.forename: C T
authors.initials: CT
authors.lastname: Liew
authors.forename: S C
authors.initials: SC
authors.lastname: Chung
mesh_terms: D000230:Adenocarcinoma / Q000201:enzymology / Q000382:microbiology* / Q000473:pathology / Q000601:surgery; D000368:Aged; D002273:Carcinogens / Q000378:metabolism; D002277:Carcinoma / Q000201:enzymology / Q000382:microbiology; D016022:Case-Control Studies; D004415:Dyspepsia / Q000201:enzymology / Q000382:microbiology; D005091:Exons / Q000235:genetics; D005260:Female; D005743:Gastrectomy; D017353:Gene Deletion; D005838:Genotype; D005982:Glutathione Transferase / Q000235:genetics* / Q000378:metabolism; D016481:Helicobacter Infections; D016480:Helicobacter pylori / Q000201:enzymology* / Q000235:genetics; D006801:Humans; D008658:Inactivation, Metabolic; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000201:enzymology / Q000382:microbiology* / Q000473:pathology / Q000601:surgery
chemical_list: D002273:Carcinogens; D012333:RNA, Messenger; D005982:Glutathione Transferase