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Selective Retention of Estrogen Isomers in Estrogen-dependent Breast Tumors of Rats Demonstrated by in Vitro Methods¹

Department of Pharmacology, University of Uppsala, Uppsala, Sweden

Huggins' rat mammary tumors were induced by treatment with 7,12-dimethylbenz(a)anthracene (DMBA) and the estrogen-dependent ones were selected. The tumors avidly took up the potent estrogens 17β-estradiol and meso-hexestrol in vivo, but they did not take up the much less estrogenic racemic hexestrol. The potent estrogens in the tumor were not easily washed out in vitro. Diaphragm neither took up nor retained potent estrogens significantly.

The selectivity in vitro was most clearly visible as a selective retention of the potent estrogens in the tumor. When tumor slices and diaphragm strips were incubated with labeled 17β-estradiol, the tumor/diaphragm concentration ratios became about 2; but after a subsequent wash-out, in the presence of a large excess unlabeled 17β-estradiol, the concentration ratios increased to about 4. meso-Hexestrol, but not the less estrogenic racemic hexestrol, was selectively retained by the tumor in the same way. Unlabeled 17-estradiol, 17β-estradiol, the synthetic estrogens meso-hexestrol, racemic hexestrol, or the demethylated analog of the estrogenic acid, methallenestril, suppressed the retention of labeled 17β-estradiol by the tumor but not by the diaphragm when present during uptake. These estrogenic stereoisomers were inhibitory to an extent which was correlated with their estrogenic potencies. The degree of uptake and retention of 17β-estradiol in the tumor was diminished by a sulfhydryl inhibitor, N-ethylmaleimide, present during uptake or wash-out. The uptake of 17β-estradiol by adipose tissue was high, but showed no specificity.

In all these respects the selectivity of estrogen uptake and retention in the DMBA tumor is similar to that of the mouse uterus. This similarity indicates the presence of specific estrogen receptors in the tumor and favors the view that estrogens exert a direct influence on the growth of this tumor.

¹ Supported by the Swedish Cancer Society.

Received 5/25/67. Accepted 10/15/67.

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