The two main pathways for metabolizing estrogen are via 1 6a-hydroxylation and 2-hydroxylation.The 16a-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 16a-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-OHEl) to 16a-hydroxyestrone (16a-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 (El), 17,Bestradiol (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-OHE, to 1 6a-OHE1 was 12% lower in the cases (p=0.58).However, urinary El was 30% higher (p=0.10),E2 was 58% higher (p=0.07),E3 was 15% higher (p=0.48), and the sum of El, 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-OHE1/16a-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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Ursin et al. (1997) studied this question.
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