JNCI Journal of the National Cancer Institute

JNCI Journal of the National Cancer Institute 1999 91(12):1067-1072; doi:10.1093/jnci/91.12.1067
© 1999 by Oxford University Press

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Journal of the National Cancer Institute, Vol. 91, No. 12, 1067-1072, June 16, 1999
© 1999 Oxford University Press

REPORTS

Urinary 2-Hydroxyestrone/16-Hydroxyestrone Ratio and Risk of Breast Cancer in Postmenopausal Women

Giske Ursin, Stephanie London, Frank Z. Stanczyk, Elisabet Gentzschein, Annlia Paganini-Hill, Ronald K. Ross, Malcolm C. Pike

Affiliations of authors: G. Ursin, A. Paganini-Hill, R. K Ross, M. C. Pike, Department of Preventive Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles; S. London, National Institute of Environmental Health Sciences, Research Triangle Park, NC; F. Z. Stanczyk, E. Gentzschein, Department of Obstetrics and Gynecology, University of Southern California/Los Angeles County Women's Hospital. .

Correspondence to: Giske Ursin, M.D., Ph.D., Department of Preventive Medicine, University of Southern California/Norris Comprehensive Cancer Center, 1441 Eastlake Ave., MS #44, Suite 4407, Los Angeles, CA 90033.

BACKGROUND: It has been suggested that women who metabolize a larger proportion of their endogenous estrogen via the 16-hydroxylation pathway may be at elevated risk of breast cancer compared with women who metabolize proportionally more estrogen via the 2-hydroxylation pathway. However, the supporting epidemiologic data are scant. Consequently, we compared the ratio of urinary 2-hydroxyestrone (2-OHE₁) to 16-hydroxyestrone (16-OHE₁) in postmenopausal women with breast cancer and in healthy control subjects. METHODS: Estrogen metabolites were measured in urine samples obtained from white women who had participated in a previous population-based, breast cancer case-control study at our institution. All P values are from two-sided tests. RESULTS: All of the urinary estrogens measured, with the exception of estriol, were higher in the 66 case patients than in the 76 control subjects. The mean value of urinary 2-OHE₁ in case patients was 13.8% (P = .20) higher than that in control subjects, 16-OHE₁ was 12.1% (P = .23) higher, estrone was 20.9% higher (P = .14), and 17ß-estradiol was 12.0% higher (P = .36). The ratio of 2-OHE₁ to 16-OHE₁ was 1.1% higher in the patients (P = .84), contrary to the hypothesis. Compared with women in the lowest third of the values for the ratio of urinary 2-OHE₁ to 16-OHE₁, women in the highest third were at a nonstatistically significantly increased risk of breast cancer (odds ratio = 1.13; 95% confidence interval = 0.46-2.78), again contrary to the hypothesis. CONCLUSION: This study does not support the hypothesis that the ratio of the two hydroxylated metabolites (2-OHE₁/16-OHE₁) is an important risk factor for breast cancer.

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