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At least 19 recordsLinked to original sources
PubMed1979

Cancer of the breast. Endocrine and hormonal therapy.

Additive hormonal therapy remains the treatment of choice for disseminated breast cancer in postmenopausal women. Patients with hormone-dependent tumors receive excellent and long-lasting palliation from alterations in the hormonal milieu. Now that hormone receptor assays are clinically available, responses can be accuratedly predicted in a large percentage of cases. Tables 11--6 is a summary of additive hormonal therapy in postmenopausal patients. Endocrine ablative therapy remains of primary importance in premenopausal women because of the superior results, but androgens or antiestrogens may be helpful when patients are not surgical candidates. Castration continues to be the initial approach, with adrenalectomy or hypophysectomy reserved for promising candidates. In postmenopausal women the initial choice is estrogens. The exceptions are those patients with metastases limited to bone, when androgens excel because of an equivalent objective response and superior subjective and metabolic effects. Patients who respond to estrogens and then progress are observed for a rebound regression following the discontinuation of estrogen therapy. Whereas some who do not respond to androgens will respond to estrogens, the converse does not appear to be true (Kennedy, 1974). Currently progestins are the secondary hormonal agent of choice in postmenopausal women, but they may be displaced by antiestrogens as more data become available. In general, if a patient's tumor lacks estrogen receptors or the patient fails to respond to an adequate trial of endocrine or hormonal therapy, one should proceed directly to cytotoxic chemotherapy. A suggested plan for the integration of endocrine with hormonal therapy and both with other forms of palliation is diagrammed at the end of Chapter 12.

Adrenal Cortex Hormones↗
PubMed1976

Oral contraceptives.

Variations in the side chains attached to the gonadal hormones can produce marked changes in the potency of these compounds and can even change their predominant actions. Modification of testosterone renders it less androgenic and greatly enhances its progestational effect. The antifertility action of oral contraceptives may be exerted through any of several mechanisms: supression of follicular development, suppression of ovum expulsion or changes in endometrium or cervical mucus.

Anemia↗
PubMed1979

Interaction of drugs, hormones, and nutrition in the causes of cancer.

Hormones may act as promoters in the carcinogenic process, and occasionally their metabolites may act as antihormones or have new physiologic effects. Drugs can interact with the endocrine system in many ways. They can promote secretion of a hormone, alter its rate of removal from plasma, change plasma protein-binding characteristics, or modify routes of metabolism. Estrogens have a preparative effect on the uterine endometrium. There are biologic, clinical and epidemiologic reasons for believing that estrogen administration to postmenopausal women increases the risk for endometrial cancer. Although there are similar biologic reasons to associate prolonged estrogenic stimulation with breast cancerr, evidence for such an association is weak. Oral contraceptive use has been associated with a variety of hepatocellular tumors. Although estrogens, per se, can effect several hepatic functions, it seems likely that the 17 alpha-alkyl and 17 alpha-ethinyl functions of the progestins and estrogens are involved in this process. The role of estrogen use during pregnancy in the causation of vaginal cancer in female offspring and the role of androgens in prostate cancer have been discussed.

Anovulation↗
PubMed1979

[Current status in the treatment of breast cancer. I. Endocrine management--change of concepts and outlook for the future (author's transl)].

A renewal of interest in endocrine therapy of breast cancer is resulting from the demonstration of steroid hormone receptors in tumor cells sensitive to antiestrogens and the possibility for predicting endocrine responsiveness. Therefore new therapeutical concepts have been developed and some of the established endocrine regimens have been reduced to historical interest. It is more than doubtful that the present schematization in selecting the proper kind of endocrine treatment has any future as methodical difficulties in demonstrating hormone receptors will be overcome and the understanding of their biological function will increase.

Adrenal Cortex Hormones↗
PubMed1992

Mechanisms of hormonal and antihormonal action of contraceptive progestins at the molecular level.

19-Nor synthetic progestins undergo extensive metabolism at the target cells. The resulting metabolic conversion products interact with putative steroid receptors within the cells, and through those interactions, they may exert either agonistic, synergistic and antagonistic hormonal effects. Studies conducted in our laboratories have disclosed that norethisterone (NET) and D-(1) norgestrel (LNG), two widely used contraceptive progestins, are biotransformed to several A-ring reduced (dihydro and tetrahydro) derivatives. The resulting metabolites 5 alpha-dihydro NET (5 alpha-NET) and 5 alpha-dihydro LNG bind with relative high affinity to the progesterone and androgen receptors. To gain insight into the underlying molecular events mediating the mode of action of NET and its neutral metabolites, we have examined the expression of their biological effects at target organs by using the rabbit uteroglobin gene model and the beta-glucuronidase activity of the mouse kidney. The results of a series of experiments seem to indicate that the enzyme-mediated formation of the 5 alpha (trans A/B ring junction) NET derivative results in a significant diminution of its progestational and androgenic potencies. Furthermore, 5 alpha-NET acquire a potent anti-progestational/contragestational effect as assessed in the female rabbit. These results demonstrated that 5 alpha-reduction of 19-nor progestins exerts a paradoxical effect, at least in terms of their hormone-like effects. The overall data are in line with the concept that metabolism of synthetic progestins at hormone-sensitive organs modulates their mechanisms of action.

Animals↗
PubMed1977

Androgenic, synandrogenic, and antiandrogenic actions of progestins.

In addition to their action on the uterus and vagina, progestins exert diverse metabolic effects on a variety of tissues. These actions include androgenic, synandrogenic, and antiandrogenic effects on androgen-responsive tissues of rats and mice. The androgenic and antiandrogenic effects of progestins have been demonstrated in multiple tissues. These actions appear to be mediated via the androgen receptor. A synandrogenic effect of progestins has also been detected in some tissues. However, there are few data to indicate how this response is mediated. Progestins may also alter androgen action indirectly through changes in steroid synthesis and metabolism. The overall biologic effect of a steroid may thus be determined by the sum of its actions on a variety of tissues.

Androgen Antagonists↗