title: A pilot study of urinary estrogen metabolites (16alpha-OHE1 and 2-OHE1) in postmenopausal women with and without breast cancer.
abstract: The two main pathways for metabolizing estrogen are via 16alpha-hydroxylation and 2-hydroxylation. The 16alpha-hydroxy metabolites are biologically active; the 2-hydroxy metabolites are not. It is suggested that women who metabolize a larger proportion of their endogenous estrogen via the 16alpha-hydroxy pathway may be at significantly elevated risk of breast cancer compared with women who metabolize proportionally more estrogen via the 2-hydroxy pathway. In particular, it is suggested that the ratio of urinary 2-hydroxyestrone (2-OHE1) to 16alpha-hydroxyestrone (16alpha-OHE1) is an index of reduced breast cancer risk. This pilot study compared this ratio in postmenopausal women diagnosed with breast cancer to those of healthy controls. Urinary concentrations of estrone (E1), 17beta-estradiol (E2) and estriol (E3) were also quantified. White women who were subjects in a previous breast cancer case-control study at our institution were eligible for inclusion. All participants provided a sample of their first morning urine. The results from the first 25 cases and 23 controls are presented here. The ratio of 2-OHE1 to 16alpha-OHE1 was 12% lower in the cases (p=0.58). However, urinary E1 was 30% higher (p=0.10), E2 was 58% higher (p=0.07), E3 was 15% higher (p=0.48), and the sum of E1, E2, and E3 was 22% higher (p=0.16) in the cases. These preliminary results do not support the hypothesis that the ratio of the two hydroxylation metabolites (2-OHE1/16alpha-OHE1) is an important risk factor for breast cancer or that it is a better predictor of breast cancer risk than levels of E1, E2 and E3 measured in urine.
authors.affiliation: Department of Preventive Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles 90033-0800, USA. gursin@hsc.nsc.edu
authors.forename: G
authors.initials: G
authors.lastname: Ursin
authors.forename: S
authors.initials: S
authors.lastname: London
authors.forename: F Z
authors.initials: FZ
authors.lastname: Stanczyk
authors.forename: E
authors.initials: E
authors.lastname: Gentzschein
authors.forename: A
authors.initials: A
authors.lastname: Paganini-Hill
authors.forename: R K
authors.initials: RK
authors.lastname: Ross
authors.forename: M C
authors.initials: MC
authors.lastname: Pike
mesh_terms: D001943:Breast Neoplasms / Q000209:etiology / Q000652:urine*; D016022:Case-Control Studies; D004958:Estradiol / Q000652:urine; D004964:Estriol / Q000652:urine; D004970:Estrone / Q000652:urine; D005260:Female; D006801:Humans; D006894:Hydroxyestrones / Q000652:urine*; D008593:Menopause; D008875:Middle Aged; D009376:Neoplasms, Hormone-Dependent / Q000209:etiology / Q000652:urine*; D010865:Pilot Projects; D012307:Risk Factors; D039181:Steroid 16-alpha-Hydroxylase
chemical_list: D006894:Hydroxyestrones; C026702:16-hydroxyestrone; D004970:Estrone; D004958:Estradiol; D039181:Steroid 16-alpha-Hydroxylase; D004964:Estriol; C024980:2-hydroxyestrone