GENETIC POLYMORPHISMS OF THE CANCER-RELATED GENE AND HELICOBACTER-PYLORI INFECTION IN JAPANESE GASTRIC-CANCER PATIENTS AN AGE AND GENDER MATCHED CASE-CONTROL STUDY

BACKGROUND. Gastric cancer is a multistage process, each caused by num erous factors. The objective of this study was to elucidate the risk f actors for gastric cancer by using molecular epidemiologic techniques and serum markers. METHODS. Serum pepsinogen I levels, pepsinogen I/pe psinogen II (I/II) ratios, serum IgG antibody against Helicobacter pyl ori (H. pylori), and genetic polymorphisms of cytochrome p450 2E1 (CYP 2E1), glutathione-S-transferase M1 (GSTM1), and L-myc protooncogenes w ere 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 per formed to elucidate which risk factors for gastric cancer were contrib uting the most to gastric carcinogenicity. RESULTS. Serum pepsinogen I level (odds ratio [OR] = 1.81; 95% confidence interval [CI], 1.04-3.1 6) and pepsinogen I/II ratios (OR = 3.09; 95% CI, 1.74-5.49) were sign ificantly associated with gastric cancer risk in a case-control study. Seropositivity of serum IgG antibody against H. pylori (OR = 1.25; 95 % CI, 0.84-1.85) and specific genotypes of a L-myc genetic polymorphis m (OR = 1.33; 95% CI, 0.59-2.99) were more commonly observed in gastri c cancer cases, but this was not statistically significant. Specific g enotypes of the CYP2E1 RsaI polymorphism and GSTM1 gene deletion were not associated with gastric cancer. CONCLUSIONS. Atrophic mucosal chan ge, indicated by serum pepsinogen levels, is possible a risk factor fo r gastric cancer. X. pylori infection and genetic polymorphisms of CYP 2E1, L-myc, and GSTM1 genetic polymorphisms were not risk factors in t his study. (C) 1996 American Cancer Society.