Control of hormone receptor levels and growth of 7,12-dimethylbenz(a)anthracene-induced mammary tumors by estrogens, progesterone and prolactin.
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 5½ 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.
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DMBA-induced mammary carcinoma in the rat has been widely used as a model of hormone-sensitive breast cancer in women.
“The DMBA-induced mammary carcinoma in the rat has been widely used as a model of hormone-sensitive breast cancer in women (242,256,257).”
From Endocrine and intracrine sources of androgens in women: inhibition of breast cancer and other roles of androgens and their precursor dehydroepiandrosterone (2003) · cites this paper as [257]
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“The DMBA-induced mammary carcinoma in the rat has been widely used as a model of hormone-sensitive breast cancer in women (242, 256, 257).”
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Self-citation
- Authors
- ASSELIN, J., KELLY, P. A., CARON, M. G., & LABRIE, F.
- Affiliations
- Centre hospitalier de l'Université Laval (CA)
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 1977-09
- Volume
- 101
- Issue
- 3
- Pages
- 666-671
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2099985701
- Cited by
- 73
- References
- 0
- Citations by year
- 2016: 1
- FWCI
- 3.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Keywords
- DMBA-induced mammary tumors, estrogen receptor, progesterone receptor, prolactin receptor, estradiol, hormone-dependent tumors, ovariectomy, tumor growth, hormone binding, combined hormone therapy, estrogen-progesterone interaction
- MeSH terms
- Animals, Castration, Estradiol, Female, Mammary Neoplasms, Experimental, Norpregnadienes, Progesterone, Protein Binding, Receptors, Cell Surface, 9,10-Dimethyl-1,2-benzanthracene, Progesterone Congeners, Rats
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