NDLI: Lack of association between the functional polymorphisms in the estrogen-metabolizing genes and risk for hepatocellular carcinoma.

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Lack of association between the functional polymorphisms in the estrogen-metabolizing genes and risk for hepatocellular carcinoma.

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Lack of association between the functional polymorphisms in the estrogen-metabolizing genes and risk for hepatocellular carcinoma.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yuan, Xiaoyan Zhou, Gangqiao Zhai, Yun Xie, Weimin Cui, Ying Cao, Jia Zhi, Lianteng Zhang, Hongxing Yang, Hao Zhang, Xiaoai Qiu, Wei Peng, Yong Zhang, Xiumei Yu, Ling Xia, Xia He, Fuchu
Description	Country affiliation: China Author Affiliation: Yuan X ( The State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing 100850, China.)
Abstract	Estrogens have been proposed to act as tumor promoters and induce hepatocarcinogenesis. Recently, we observed a significant association between the risk for hepatocellular carcinoma and the polymorphisms of the estrogen receptor (ESR) alpha (ESR1) gene, supporting the hypothesis of involvement for the estrogen-ESR axis in the estrogen-induced hepatocarcinogenesis. In this study, based on another hypothesis in which estrogen metabolites can directly cause DNA damage and affect tumor initiation, we examined whether the polymorphisms of the estrogen-metabolizing enzymes (EME), which are involved in biogenesis (CYP17, CYP19), bioavailability (CYP1A1, CYP1B1), and degradation (catechol-O-methyltransferase) of the estrogens, have any bearing on the risk for hepatocellular carcinoma. Seven functional polymorphisms in five EMEs (CYP17 MspAI site, CYP19 Trp39Arg, Ile462Val and MspI site in CYP1A1, CYP1B1 Val432Leu, and Ala72Ser and Val158Met in catechol-O-methyltransferase) were genotyped in 434 patients with hepatocellular carcinoma and 480 controls by PCR-RFLP analysis. The associations between the polymorphisms and hepatocellular carcinoma risk were evaluated while controlling for confounding factors. No significant association with the risk for hepatocellular carcinoma was observed with the seven polymorphisms in hepatitis B virus carriers and non-hepatitis B virus carriers after correction for multiple comparisons. After stratification by common confounding factors of hepatocellular carcinoma, the EME polymorphism remained no significant association with the hepatocellular carcinoma risk. Furthermore, no signs of gene-gene interactions were observed for each combination of the seven polymorphisms. Our findings suggest that the polymorphisms of EMEs may not contribute significantly to the risk for hepatocellular carcinoma.
File Format	HTM / HTML
ISSN	10559965
e-ISSN	15387755
Journal	Cancer Epidemiology Biomarkers & Prevention
Issue Number	12
Volume Number	17
Language	English
Publisher	American Association for Cancer Research
Publisher Date	2008-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cancer epidemiology Carcinoma, Hepatocellular Genetics Estrogens Metabolism Liver Neoplasms Polymorphism, Genetic Aromatase Aryl Hydrocarbon Hydroxylases Enzymology Case-control Studies Catechol O-methyltransferase Cytochrome P-450 Cyp1a1 Cytochrome P-450 Cyp1b1 Genotype Haplotypes Polymerase Chain Reaction Polymorphism, Restriction Fragment Length Steroid 17-alpha-hydroxylase Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Epidemiology Oncology

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