https://scholars.lib.ntu.edu.tw/handle/123456789/568751
標題: | Polymorphisms in XRCC1 and glutathione S-transferase genes and hepatitis B-related hepatocellular carcinoma | 作者: | MING-WHEI YU Yang S.-Y. Pan I.-J. Lin C.-L. CHUN-JEN LIU Liaw Y.-F. Lin S.-M. PEI-JER CHEN Lee S.-D. Chen C.-J. |
公開日期: | 2003 | 出版社: | Oxford University Press | 卷: | 95 | 期: | 19 | 起(迄)頁: | 1485-1488 | 來源出版物: | Journal of the National Cancer Institute | 摘要: | Chronic infection with hepatitis B virus (HBV) causes DNA damage. An arginine (Arg)-to-glutamine (Gln) polymorphism at codon 399 in the XRCC1 gene is putatively associated with DNA damage. In a case-control study of 577 HBV surface antigen carriers with hepatocellular carcinoma (HCC) and 389 HBV carrier control subjects, we investigated the association between this polymorphism and the risk of HCC and assessed whether this association varied with glutathione S-transferase (GST) status; GSTs are involved in carcinogen metabolism. All statistical tests were two-sided. The XRCC1 Gln allele was associated with a dose-dependent increased risk of early-onset HCC (<50 years) but not with the risk of late-onset HCC (Ptrend = .01). The GSTT1-null genotype alone did not affect risk, but the GSTM1-null genotype was associated with a decreased risk for early-onset HCC. Various combinations of GSTM1 and GSTT1 genotypes differentially modified the association of XRCC1 with HCC (Pinteraction = .005); e.g., for individuals with the GSTT1-null/ GSTM1-present genotype, the risk of HCC was greater for those with the Gln/Gln genotype (odds ratio = 8.07, 95% confidence interval = 1.67 to 38.93) than for those with the Arg/Arg genotype. Thus, GST status appears to affect the risk of HCC associated with this XRCC1 polymorphism. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-0141763753&doi=10.1093%2fjnci%2fdjg051&partnerID=40&md5=a49ce23f9c995f4534307148d6cb963d https://scholars.lib.ntu.edu.tw/handle/123456789/568751 |
ISSN: | 0027-8874 | DOI: | 10.1093/jnci/djg051 | SDG/關鍵字: | arginine; carcinogen; gene product; glutamine; glutathione transferase; hepatitis B surface antigen; protein XRCC1; unclassified drug; DNA binding protein; glutathione transferase; X ray repair cross complementing protein 1; X-ray repair cross complementing protein 1; adult; aged; allele; article; cancer risk; chronic hepatitis; codon; confidence interval; DNA damage; DNA polymorphism; female; gene dosage; genetic association; genotype; hepatitis B; Hepatitis B virus; human; liver cell carcinoma; male; null allele; priority journal; risk assessment; statistical analysis; virus carrier; case control study; DNA repair; genetic polymorphism; genetics; hepatitis B; liver cell carcinoma; liver tumor; risk; risk factor; virology; Carcinoma, Hepatocellular; Case-Control Studies; DNA Repair; DNA-Binding Proteins; Genotype; Glutathione Transferase; Hepatitis B; Humans; Liver Neoplasms; Odds Ratio; Polymorphism, Genetic; Risk Assessment; Risk Factors |
顯示於: | 臨床醫學研究所 |
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