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Genetic polymorphisms of the cancer related gene and Helicobacter pylori infection in Japanese gastric cancer patients: An age and gender matched case–control study
Author(s) -
Kato Shunji,
Onda Masahiko,
Matsukura Norio,
Tokunaga Akira,
Matsuda Noriko,
Yamashita Kiyohiko,
Shields Peter G.
Publication year - 1996
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/(sici)1097-0142(19960415)77:8+<1654::aid-cncr11>3.0.co;2-x
Subject(s) - medicine , cancer , gene , case control study , oncology , genetics , biology
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 II (I/II) ratios, serum IgG antibody against Helicobacter pylori ( H. pylori ), and genetic polymorphisms of cytochrome p450 2E1 (CYP2E1), glutathione‐S‐transferase M1 (GSTM1), 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 I/II ratios (OR = 3.09; 95% CI, 1.74–5.49) were significantly 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 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 CYP2E1 RsaI polymorphism and GSTM1 gene deletion were not associated with gastric cancer. CONCLUSIONS Atrophic mucosal change, indicated by serum pepsinogen levels, is possible a risk factor for gastric cancer. H. pylori infection and genetic polymorphisms of CYP2E1, L‐ myc, and GSTM1 genetic polymorphisms were not risk factors in this study. Cancer 1996;77:1654‐61.