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1 Department of Epidemiology and Population Studies, Collegium Medicum and 2 Department of General Biochemistry, Faculty of Biotechnology, Jagiellonian University, Kraków, Poland; 3 Radcliffe Institute for Advanced Study and 4 Department of Anthropology, Harvard University, Cambridge, Massachusetts; 5 Department of Community Medicine, University of Tromso, Norway; and 6 Ulleval University Hospital, Oslo, Norway
Requests for reprints: Grazyna Jasienska, Department of Epidemiology and Population Studies, Collegium Medicum, Jagiellonian University, Grzegórzecka 20, 31-531 Kraków, Poland. Phone: 48-12-424-1380. E-mail: jasienska{at}post.harvard.edu
Variation in the levels of sex-steroid hormones results from differences in developmental conditions, adult lifestyle, and genetic polymorphism. Genes involved in sex-steroid biosynthesis have been implicated to influence levels of hormones in premenopausal women, but the results were inconclusive. We tested variation among women in levels of salivary estradiol (E2) corresponding to CYP17 genotypes. CYP17 encodes cytochrome P450c17
, which mediates two enzymes important in E2 synthesis. In contrast to the earlier studies that relied on one or a few samples for assessing the E2 levels of an individual woman, our study is based on daily collected saliva samples for one entire menstrual cycle. Sixty Polish women, ages 24 to 36 years, with regular menstrual cycles and no reported fertility problems participated in the study. Women with A2/A2 genotype had 54% higher mean E2 levels than women with A1/A1 genotype (P = 0.0001) and 37% higher than women with A1/A2 genotype (P = 0.0008). Heterozygous A1/A2 women had 13 % higher E2 levels than homozygous A1/A1 women (but this difference was significant only in a nonparametric test). Levels of E2 during the day with highest E2 (day 1) were 72% higher in A2/A2 compared with A1/A1 (P = 0.01) and 52 % higher compared with A1/A2 (P = 0.03). Our results suggest that CYP17 genotype may serve as a biomarker of endocrine function in women of reproductive age. (Cancer Epidemiol Biomarkers Prev 2006;15(11):21315)
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