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Control of Hormone Receptor Levels and Growth of 7,12-Dimethylbenz(a)anthracene-Induced Mammary Tumors by Estrogens, Progesterone and Prolactin

Medical Research Council Group in Molecular Endocrinology, Le Centre Hospitalier de I'Unioersité Laval Quebec G1V 4G2, Canada

Abstract

The effect of various hormone treatments was investigated on the growth and hormone receptor levels of hormone-dependent (those which regressed after ovariectomy) dimethylbenz- (a)anthracene (DMBA)-induced mammary tumors in the rat. Hormone binding measured in die tumors which remained 5 weeks after ovariectomy was low for estradiol-17β (E2) (0.6 ± 0.2 pmol/g tissue), R 5020 (0.9 ± 0.4 pmol/g tissue) and prolactin (PRL) (0.9 ± 0.4% of specific binding). In non-castrated animals, binding values were 2.9 ± 0.4 pmol/g tissue, 13.7 ± 2.0 pmol/g tissue and 3.2 ± 0.3% for E₂, R 5020 and PRL, respectively. Administration of progesterone (P) alone (0.5 mg/day) for three weeks to castrated animals had no effect on tumor size or hormone binding. Treatment with E₂ (0.5 µg/day) for the same period of time increased tumor size and hormone binding: E₂, 3.0 ± 0.7 pmol/g tissue; R 5020, 14.8 ± 3.3 pmol/g tissue; PRL, 2.4 ± 0.6%. At a daily dose of 2 mg, PRL alone increased tumor size slightly while honnone binding remained low except for that of E₂ which was increased to 2.0 ± 0.4 pmol/g tissue. Combination of E₂ with P or PRL resulted in tumor growth greater than that observed after PRL or E₂ alone. The levels of hormone binding present in the tumors at the end of these combined treatments were all increased to levels similar to those obtained with E₂ alone. It can be concluded that the presence of estrogen receptors in the DMBA-induced mammary tumors is a veiy good index of hormone dependency. In fact, the levels of this receptor were high under all honnone treatments which led to stimulation of tumor growth. These studies also clearly demonstrate that the concentration of P receptors in the DMBAinduced mammary tumors, as well as the response of the tissue to P, depends upon E₂.

Footnotes

Supported by a grant from the National Cancer Institute of Canada.

Received January 24, 1977.

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