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hOGG1 Ser326Cys Polymorphism and Lung Cancer Susceptibility¹

Department of Pathology, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan [H. S., K. N., H. I., S. B., K. S.]; Biology Division, National Cancer Center Research Institute, Tokyo 104-0045, Japan [T. K., K. S., J. Y.]; Department of Preventive Medicine, Nagoya University School of Medicine, Nagoya 466-8550, Japan [K. W., Y. O.]; National Okinawa Hospital, Okinawa 901-2214, Japan [K. G.]; Hypertension Gene Laboratory and Institute for Biomedical Research, Department of Physiology, The University of Sydney, Sydney, New South Wales 2006, Australia [B. J. M.]; Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, People’s Republic of China [C. G., Z. L., J. W.]; Epidemiology Division, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan [T. T., K. T.]; Department of Forensic Medicine, Albert Szent Gyorgyi Medical University, Kossuth L.sg1.40, Hungary [T. V.]; Department of Legal Medicine, Tokyo Women’s Medical College, Tokyo 162-8666, Japan [T. S.]; The Institute of Statistical Mathematics, Tokyo 106-8569, Japan [J. K. L.]; Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania 15261 [J. J. M.]; Epidemiology and Biostatistics Division, National Cancer Center Research Institute East, Chiba 277-8577, Japan [S. T.]; and Department of Pathology, Ryukyu University School of Medicine, Okinawa 903-0125, Japan [T. I.]

The human homologue of the yeast OGG1 gene, hOGG1, has been cloned, and its genetic structure has been determined. Several polymorphisms in the hOGG1 gene were detected in the Japanese populations, and among them, the Ser-Cys polymorphism at codon 326 has been shown to have a functional difference in complementation of mutant Escherichia coli that is defective in the repair of 8-hydroxyguanine. Activity in the repair of 8-hydroxyguanine is greater in hOGG1-Ser³²⁶ protein than in hOGG1³²⁶ protein. Because many environmental carcinogens produce 8-hydroxyguanine residue and mismatching to this modified base potentially causes oncogenic mutations, the capacity to repair these lesions can be involved in cancer susceptibility in human beings. We, therefore, examined allele distributions of the Ser326Cys polymorphism in a case-control study of male lung cancer in Okinawa. The analyses based on 241 cases and 197 hospital controls disclosed the following findings. (a) Those with the Cys/Cys genotype were at an increased risk of squamous cell carcinoma and nonadenocarcinoma compared to those with the Ser/Cys and those with the Ser/Ser genotypes combined. The odds ratios adjusted for age and smoking history were 3.01 (95% confidence interval, 1.33–6.83) and 2.18 (95% confidence interval, 1.05–4.54), respectively. (b) The odds ratios for other histological subtypes of lung cancer or those in total were not significant. Those for Cys/Cys or Ser/Cys genotype against Ser/Ser did not reach statistical significance in any cell type. (c) The distributions of this polymorphism varied for different populations (Chinese, Japanese, Micronesians, Melanesians, Hungarians, and Australian Caucasians), with much less prevalence of Cys allele in the latter three populations. Although our sample size was limited, these results indicate that the Ser326Cys variant may be related to squamous cell lung cancer susceptibility. The Cys/Cys genotype appears to be more susceptible to squamous cell carcinoma, although the risk is less than that previously reported to be associated with the CYPIA1 gene. Further studies are needed to assess the importance of the interpopulation variation to cancer susceptibility.

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