Abstract 1335: Association between polymorphisms of APE1 and OGG1 genes and risk of colorectal cancer in Taiwan.

Abstract

Abstract Background: Colorectal cancer (CRC) is the third leading cause of cancer death in Taiwan. Previous studies indicated that oxidative damages resulting from reactive oxygen species (ROS) generation participate in all stages of the cancer process. Mutagenic 8-hydroxy-2’-deoxyguanosine, one of the major DNA lesions generated by ROS, is preferentially repaired by 8-oxoguanine glycosylase I (OGG1) and apurinic-apyrimidinic endonuclease 1 (APE1). Since polymorphisms of OGG1 S326C, R154H and APE1 D148E, T-656G were associated with the enzyme activities, this study was designed to evaluate the roles of the OGG1 and APE1 polymorphisms in CRC risk. Method: We recruited 727 newly diagnosed colorectal adenocarcinoma cases and 736 age- and sex-matched healthy controls in a medical center. Genomic DNA isolated from buffy coat was used for genotyping by PCR methods. Because the frequency of the sequence variants of OGG1 R154H was too low (H allele was 0.14%), this polymorphism was excluded in further data analysis. Unconditional logistic regressions were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). Results: Subjects with OGG1 326 Ser/Cys genotype had an increased CRC risk (OR = 1.47; 95% CI = 1.06-2.04) compared to those carrying the Ser/Ser genotype, particularly among individuals aged more than 60 years (OR = 1.60, 95% CI = 1.02-2.05). However, there was no significant association between APE1 polymorphisms and CRC risk. Conclusion: Our results indicated that OGG1 S326C polymorphism may associate with CRC risk in Taiwanese population, whereas APE1 polymorphisms may not modulate this disease risk. Citation Format: Chih-Ching Yeh, Ling-Ling Hsieh, Reiping Tang. Association between polymorphisms of APE1 and OGG1 genes and risk of colorectal cancer in Taiwan. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1335. doi:10.1158/1538-7445.AM2013-1335