Environ Health Perspect. 1997 Apr;105(Suppl 3):601–605. doi:
A pilot study of urinary estrogen metabolites (16alpha-OHE1 and 2-OHE1) in postmenopausal women with and without breast cancer.
G Ursin
1Department of Preventive Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles 90033-0800, USA. [email protected] articles by
1,
S London
1Department of Preventive Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles 90033-0800, USA. [email protected] articles by
1,
F Z Stanczyk
1Department of Preventive Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles 90033-0800, USA. [email protected] articles by
1,
E Gentzschein
1Department of Preventive Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles 90033-0800, USA. [email protected] articles by
1,
A Paganini-Hill
1Department of Preventive Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles 90033-0800, USA. [email protected] articles by
1,
R K Ross
1Department of Preventive Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles 90033-0800, USA. [email protected] articles by
1,
M C Pike
1Department of Preventive Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles 90033-0800, USA. [email protected] articles by
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1Department of Preventive Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles 90033-0800, USA. [email protected]
PMCID: PMC1469909 PMID:
See letter "
" in volume 106 on page A126c.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.
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Selected References
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