An-Kuo Chou1, Ming-Yi Shen2,3, Fang-Yu Chen2, Chieh-Lun Hsiao3,4, Liang-Chun Shih4, Wen-Shin Chang4, Chia-Wen Tsai4, Tsung-Ho Ying5, Ming-Hsien Wu6, Chung-Yu Huang7, DA-Tian Bau8,4,9. 1. Department of Anesthesiology, China Medical University Hospital, Taichung, Taiwan, R.O.C. 2. Department of Medical Research, China Medical University Hospital, Taichung, Taiwan Hospital, Taichung, Taiwan, R.O.C. 3. Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan, R.O.C. 4. Terry Fox Cancer Research Laboratory, China Medical University Hospital, Taichung, Taiwan, R.O.C. 5. Department of Obstetrics and Gynecology, Chung Shan Medical University Hospital, Taichung, Taiwan, R.O.C. 6. Taichung Armed Forces General Hospital, Taichung, Taiwan, R.O.C. 7. Taoyuan Armed Forces General Hospital, Taoyuan, Taiwan, R.O.C. 8. Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan, R.O.C. datian@mail.cmuh.org.tw artbau2@gmail.com. 9. Department of Bioinformatics and Medical Engineering, Asia University, Taichung, Taiwan, R.O.C.
Abstract
BACKGROUND/AIM: Flap endonuclease 1 (FEN1), a protein with multiple functions in genome stability maintenance, is important in cancer prevention. The two functional germline variants of FEN1, rs174538 and rs4246215, regarding cancer susceptibility have been reported in lung, breast, liver, esophageal, gastric, colorectal cancer, glioma and leukemia, but not endometriosis. In this study, we firstly aimed at evaluating the contribution of FEN1 genotypes to endometriosis risk in a representative Taiwan population. MATERIALS AND METHODS: In total, 153 patients with endometriosis and 636 non-cancer healthy controls were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methodology. RESULTS: The genotypes of FEN1 rs174538, but not those of rs4246215, were differently distributed between the endometriosis and control groups. In detail, the AA of FEN1 rs174538 genotypes were significantly less frequently found among endometriosis patients than among controls (odds ratio [OR]=0.43, 95% confidence interval [CI]=0.24-0.78, p=0.0125). The A allele at FEN1 rs174538 was also significantly less frequent among cases than controls (OR=0.65, 95%CI=0.50-0.86, p=0.0021). As for age of first menarche, those with first menarche at the age >12.8 carrying the FEN1 rs174538 AA genotype conferred lower OR of 0.29 (95%CI=0.11-0.78, p=0.0381) for endometriosis. Regarding the full pregnancy status, those without having had a full-term pregnancy carrying the FEN1 rs174538 AA genotype were of lower risk (ORs=0.12, 95%CI=0.03-0.53, p=0.0050). CONCLUSION: The FEN1 rs174538 A allele is a novel protective biomarker for endometriosis and this genotype may have interactions with age- and hormone-related factors on the development of endometriosis. Copyright
BACKGROUND/AIM: Flap endonuclease 1 (FEN1), a protein with multiple functions in genome stability maintenance, is important in cancer prevention. The two functional germline variants of FEN1, rs174538 and rs4246215, regarding cancer susceptibility have been reported in lung, breast, liver, esophageal, gastric, colorectal cancer, glioma and leukemia, but not endometriosis. In this study, we firstly aimed at evaluating the contribution of FEN1 genotypes to endometriosis risk in a representative Taiwan population. MATERIALS AND METHODS: In total, 153 patients with endometriosis and 636 non-cancer healthy controls were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methodology. RESULTS: The genotypes of FEN1rs174538, but not those of rs4246215, were differently distributed between the endometriosis and control groups. In detail, the AA of FEN1rs174538 genotypes were significantly less frequently found among endometriosispatients than among controls (odds ratio [OR]=0.43, 95% confidence interval [CI]=0.24-0.78, p=0.0125). The A allele at FEN1rs174538 was also significantly less frequent among cases than controls (OR=0.65, 95%CI=0.50-0.86, p=0.0021). As for age of first menarche, those with first menarche at the age >12.8 carrying the FEN1rs174538 AA genotype conferred lower OR of 0.29 (95%CI=0.11-0.78, p=0.0381) for endometriosis. Regarding the full pregnancy status, those without having had a full-term pregnancy carrying the FEN1rs174538 AA genotype were of lower risk (ORs=0.12, 95%CI=0.03-0.53, p=0.0050). CONCLUSION: The FEN1rs174538 A allele is a novel protective biomarker for endometriosis and this genotype may have interactions with age- and hormone-related factors on the development of endometriosis. Copyright
Authors: D W Cramer; E Wilson; R J Stillman; M J Berger; S Belisle; I Schiff; B Albrecht; M Gibson; B V Stadel; S C Schoenbaum Journal: JAMA Date: 1986-04-11 Impact factor: 56.272
Authors: Wen-Qing Li; Nan Hu; Paula L Hyland; Ying Gao; Zhao-Ming Wang; Kai Yu; Hua Su; Chao-Yu Wang; Le-Min Wang; Stephen J Chanock; Laurie Burdett; Ti Ding; You-Lin Qiao; Jin-Hu Fan; Yuan Wang; Yi Xu; Jian-Xin Shi; Fangyi Gu; William Wheeler; Xiao-Qin Xiong; Carol Giffen; Margaret A Tucker; Sanford M Dawsey; Neal D Freedman; Christian C Abnet; Alisa M Goldstein; Philip R Taylor Journal: Carcinogenesis Date: 2013-03-15 Impact factor: 4.944