The Metabolism of Testosterone by Tissue From Normal and Neoplastic Rat Breast

King, R. J. B.; Gordon, J.; Helfenstein, Janet E.

doi:10.1677/joe.0.0290103

Cited by 18 publications

(5 citation statements)

References 13 publications

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“…Although no significant difference in steroid metabolism was detected between hormone-dependent and independent DMBA-induced rat mammary tumours (King et al, 1965) endocrine-treated animals were used and in the present study effects in such animals were more difficult to detect than in unmanipulated animals. Furthermore the levels of tumour 5ct reduction were at least 10-fold less (King et al, 1964) than those reported in the system used in the present study. It is possible that the apparent relationship detected in this study between hormone dependence and steroid metabolism is only causal and that some other feature of transplantation has caused the observed increase in testosterone metabolism.…”

Section: Tumour Growthcontrasting

confidence: 76%

Effects of serial passage on the endocrine response and steroid metabolism of a rat mammary carcinoma

Miller¹

1980

Br J Cancer

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Section: Tumour Growthcontrasting

confidence: 76%

Effects of serial passage on the endocrine response and steroid metabolism of a rat mammary carcinoma

Miller¹

1980

Br J Cancer

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“…Similar conversions are found in human breast cancer tissue [9]. Normal rat mammary gland and DMBA-induced mammary tumors have been shown in enzymatic assays to contain 17~-hydroxysteroid dehydrogenase, 3-ketosteroid reductase, and A4-5a-hydrogenase activities [29,35]. The enzymatic systems which process steroids in human breast cancer tissue are also present in DMBAinduced mammary tumors, thus supporting the use of DMBA-induced tumors as models of human breast cancer [4][5][6][7][8][9].…”

Section: Discussionmentioning

confidence: 62%

Androstenedione and androst-5-ene-3β,17β-diol stimulate DMBA-induced rat mammary tumors — role of aromatase

Dauvois

Labrie

1989

Breast Cancer Res Tr

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The effect of the adrenal steroids androst-5-ene-3 beta,17 beta-diol (delta 5-diol) and androstenedione (delta 4-dione) was studied on the growth of mammary carcinoma induced in the rat by dimethylbenz[a]anthracene (DMBA). The plasma levels of the two steroids were maintained at values within the range of those found in the circulation of post-menopausal women by constant release from osmotic pumps in ovariectomized animals. delta 5-diol and delta 4-dione, at the daily release rate of 500 micrograms, led to plasma levels of 1.26 +/- 0.19 and 1.72 +/- 0.75 ng/ml, respectively. At these physiologically relevant plasma concentrations, both delta 5-diol and delta 4-dione caused a marked stimulation of tumor growth while having minimal or no effect on uterine weight or on plasma prolactin and LH levels. Concomitant treatment with the aromatase inhibitor aminoglutethimide completely blocked the stimulatory effect of delta 4-dione released from silastic implants on tumor growth, while simultaneous administration of the antiandrogen flutamide had no significant effect. On the other hand, when aminoglutethimide was administered with delta 5-diol, the stimulatory effect of the adrenal steroid on tumor growth was not affected. Such data indicate that, under the present experimental conditions, transformation of delta 4-dione into androgens plays a minor role, the predominant effect of the adrenal steroid being stimulation of tumor growth through conversion into estrogens, while delta 5-diol exerts a direct estrogenic effect independent from aromatase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…

HUMAN and rat mammary tumours metabolize steroid hormones and thus have the capacity to modify their local hormonal environment (Adams & Wong, 1968;Jones et al, 1970;King et al, 1964;Miller et al, 1974). In previous studies, we have investigated the metabolism of testosterone by a predominantly ovary-dependent DMBA-induced mammary tumour, and have shown it to be sensitive to levels of other hormones present in vitro (Miller, 1976a), or in vivo (Miller, 1976b, c;Buchan et al, 1976).

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mentioning

confidence: 99%

Hormonal status and steroid metabolism in two transplantable rat mammary tumours

Miller¹,

Stewart²,

Hawkins³

1979

Br J Cancer

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HUMAN and rat mammary tumours metabolize steroid hormones and thus have the capacity to modify their local hormonal environment (Adams & Wong, 1968;Jones et al., 1970;King et al., 1964;Miller et al., 1974). In previous studies, we have investigated the metabolism of testosterone by a predominantly ovary-dependent DMBA-induced mammary tumour, and have shown it to be sensitive to levels of other hormones present in vitro (Miller, 1976a), or in vivo (Miller, 1976b, c;Buchan et al., 1976). We now report a study of the metabolism of androgens by ovary-independent tumours derived by transplantation. By using multiple tumours transplanted to a single rat, it has been possible to examine tumours derived from the same host animal before and after 2 endocrine manipulations.All animals were of an inbred strain of Sprague-Dawley rat, obtained from the Animal Diseases Research Association (ADRA), Moredun Institute, Edinburgh. Two lines of transplantable tumours were used: TG3 and TG5. These were histologically carcinomas, originally induced in female "ADRA" rats at 50 days of age by i.v. administration of 5 mg of DMBA. Both tumours were then serially transplanted by dorsal skin implantation of tumour fragments into neonatally-thymectomized hosts. At the time of study TG3 was at its 6th passage and TG5 was at its 7th passage.Three separate portions of a single donor tumour were implanted at different dorsal sites in each neonatally thymectomized host animal at 50 days of age. Tumours were measured twice weekly throughout the period of study. When the largest tumour reached 1 5 x 1 5 cm in size it was removed through a dorsal skin incision and the animal was immediately bilaterally oophorectomized. Ten days later, a further tumour was excised. The animals were then given daily injections of oestradiol-17f (1 jig in 0-2 ml corn oil) for a further 10 days.The remaining tumour was excised and the animals were killed, no injection of oestradiol being given on the day of death. Eight rats were so treated (4 with TG3 tumours and 4 with TG5 tumours). Control animals (2 with TG3 tumours and 2 with TG5 tumours) were treated similarly except that a sham oophorectomy was performed in place of an oophorectomy and the injection vehicle replaced oestradiol.After excision, portions of each tumour (0.5 g) were used for steroid-metabolism studies. Each was finally sliced at 0°C in Krebs-Ringer phosphate buffer pH 7-4 (5 ml). An NADPH-generating system and radioactive precursor(20(lCi of either 7a(3H) dehydroepiandrosterone (DHA) or 7a(3H) testosterone) was added. The incubation systems were shaken at 37°C in an atmosphere of 02 for 2 h (TG3 series) or 1 h (TG5 series on account of the high activity found in the tumour lines). The reaction was stopped by adding methanol to 80% v/v and the incubations stored at

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The Metabolism of Testosterone by Tissue From Normal and Neoplastic Rat Breast

Cited by 18 publications

References 13 publications

Effects of serial passage on the endocrine response and steroid metabolism of a rat mammary carcinoma

Effects of serial passage on the endocrine response and steroid metabolism of a rat mammary carcinoma

Androstenedione and androst-5-ene-3β,17β-diol stimulate DMBA-induced rat mammary tumors — role of aromatase

Hormonal status and steroid metabolism in two transplantable rat mammary tumours

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