Helicobacter pylori and the null genotype of glutathione-S-transferase-mu in patients with gastric adenocarcinoma

Cancer. 1998 Jan 15;82(2):268-73. doi: 10.1002/(sici)1097-0142(19980115)82:2<268::aid-cncr4>3.0.co;2-n.


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.

Publication types

  • Comparative Study

MeSH terms

  • Adenocarcinoma / enzymology
  • Adenocarcinoma / microbiology*
  • Adenocarcinoma / pathology
  • Adenocarcinoma / surgery
  • Aged
  • Carcinogens / metabolism
  • Carcinoma / enzymology
  • Carcinoma / microbiology
  • Case-Control Studies
  • Dyspepsia / enzymology
  • Dyspepsia / microbiology
  • Exons / genetics
  • Female
  • Gastrectomy
  • Gene Deletion
  • Genotype
  • Glutathione Transferase / genetics*
  • Glutathione Transferase / metabolism
  • Helicobacter Infections*
  • Helicobacter pylori / enzymology*
  • Helicobacter pylori / genetics
  • Humans
  • Inactivation, Metabolic
  • Male
  • Middle Aged
  • Polymerase Chain Reaction
  • RNA, Messenger / analysis
  • RNA, Messenger / genetics
  • Risk Factors
  • Stomach Neoplasms / enzymology
  • Stomach Neoplasms / microbiology*
  • Stomach Neoplasms / pathology
  • Stomach Neoplasms / surgery


  • Carcinogens
  • RNA, Messenger
  • Glutathione Transferase