Genetic polymorphisms of the cancer related gene and Helicobacter pylori infection in Japanese gastric cancer patients: An age and gender matched case–control study

✍ Scribed by Shunji Kato; Masahiko Onda; Norio Matsukura; Akira Tokunaga; Noriko Matsuda; Kiyohiko Yamashita; Peter G. Shields

• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 720 KB
• Volume: 77
• Category: Article
• ISSN: 0008-543X
• DOI: 10.1002/(sici)1097-0142(19960415)77:8<1654::aid-cncr35>3.0.co;2-x

✦ Synopsis

BACKGROUND.

Gastric cancer is a multistage process, each caused by numerous factors. The objective of this study was to elucidate the risk factors for gastric cancer by using molecular epidemiologic techniques and serum markers.

METHODS.

Serum pepsinogen I levels, pepsinogen I/pepsinogen I1 (I/II) ratios, serum IgG antibody against Helicobacter pylori (H. pylorzl, and genetic polymorphisms of cytochrome p450 2E1 (CW2E1), glutathione-S-transferase M1 (GSTMI), and L-myc protooncogenes were analyzed in 82 persons with gastric cancer and in 151 age-and sex-matched controls, who were selected from 208 gastric cancer patients and 375 noncancer patients, respectively. Statistical analysis was performed to elucidate which risk factors for gastric cancer were contributing the most to gastric carcinogenicity.

RESULTS. Serum pepsinogen I level (odds ratio [OR] = 1.81; 95% confidence interval

[CI], 1.04-3.16) and pepsinogen 1\11 ratios (OR = 3.09; 95% CI, 1.74-5.49) were significantly associated with gastric cancer risk in a case-control study. Seropositivity of seruni IgG antibody against H. pylori (OR = 1.25; 95% CI, 0.84-1.85) and specific genotypes of a L-myc genetic polymorphism (OR = 1.33; 95% CI, 0.59-2.99) were more commonly observed in gastric cancer cases, but this was not statistically significant. Specific genotypes of the CYP2El Rsal polymorphism and GSTMl gene deletion were not associated with gastric cancer. CONCLUSIONS. Atrophic rnucosal change, indicated by serum pepsinogen levels, is possible a risk factor for gastric cancer. H. pylori infection and genetic polymorphisms of CYP2E1, L-rnyc, and GSTMl genetic polymorphisms were not risk factors in this study.