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Antiestrogen-binding sites in 7,12-dimethylbenz(a)anthracene-induced rat mammary tumors: relation to growth
1Department of Physiology, Faculty of Medicine, National University of Singapore.
Abstract:
We have detected specific high-affinity binding sites for nonsteroidal antiestrogens in 98% of 7,12-dimethylbenz(a)anthracene-induced rat mammary tumors. Since recent studies have suggested that these binding sites may be involved in the regulation of cell growth and proliferation, we attempted to define a possible relationship between the growth of these hormone-dependent tumors and their antiestrogen-binding site content. Rats bearing such tumors were either treated with haloperidol (to increase prolactin secretion and stimulate tumor growth) or oophorectomized (to reduce circulating estrogen concentration and suppress tumor growth). Compared with controls, haloperidol treatment clearly enhanced tumor growth while oophorectomy induced tumor regression, but neither procedure had any effect on the antiestrogen-binding site concentration. Furthermore, tumors which responded to endocrine manipulation had similar antiestrogen-binding site concentrations as tumors which did not respond. We conclude that (1) the alterations in tumor growth induced by these endocrine manipulations are probably not mediated through a change in antiestrogen-binding site concentration, and (2) the tumor concentration of these binding sites is not under estrogen or prolactin control.
Insights
High-affinity nonsteroidal antiestrogen binding sites are present in most rat mammary tumors. Tumor growth changes did not affect binding site concentration, suggesting it
Area of Science:
- Oncology
- Endocrinology
- Molecular Biology
Background:
- Specific high-affinity binding sites for nonsteroidal antiestrogens are found in 98% of 7,12-dimethylbenz(a)anthracene-induced rat mammary tumors.
- These antiestrogen-binding sites are potentially involved in regulating cell growth and proliferation.
Purpose of the Study:
- To investigate the relationship between the growth of hormone-dependent rat mammary tumors and their antiestrogen-binding site content.
- To determine if endocrine manipulation affects the concentration of these binding sites.
Main Methods:
- Inducing tumor growth with haloperidol to increase prolactin secretion.
- Suppressing tumor growth via oophorectomy to reduce estrogen levels.
- Measuring antiestrogen-binding site concentration in tumors before and after endocrine manipulation.
Main Results:
- Neither haloperidol treatment nor oophorectomy altered the concentration of antiestrogen-binding sites in rat mammary tumors.
- Tumor growth response to endocrine manipulation did not correlate with antiestrogen-binding site concentration.
- Tumors that responded to hormonal changes and those that did not had similar binding site levels.
Conclusions:
- Alterations in mammary tumor growth induced by endocrine manipulation are likely not mediated by changes in antiestrogen-binding site concentration.
- The concentration of antiestrogen-binding sites in these tumors is independent of estrogen and prolactin levels.