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SUMMARY
The uptake of simultaneously injected [3H]oestradiol and [14C]progesterone by dimethylbenzanthracene-induced mammary tumours in the rat was compared with that obtained when oestradiol was injected alone. Progesterone was not taken up and/or retained by hormone-responsive adenomata and fibroadenomata to the same extent as oestradiol, and it is suggested that the mechanism of action of progesterone is different from that of oestradiol and does not involve retention by the target tissue. Progesterone did not affect the uptake of oestradiol by hormone-responsive adenomata and fibroadenomata but there was a tendency for progesterone to increase the uptake of oestradiol and/or its free steroid metabolites by hormone-unresponsive adenomata. This could be due either to the timing of the experiments or to progesterone altering the equilibrium between oestradiol levels in blood and hormone-unresponsive tumours.
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A large proportion of mammary gland tumours induced in the rat by dimethylbenzanthracene (DMBA) are hormone-responsive and regress after ovariectomy. Such tumours possess the ability to take up and retain injected oestradiol and this may be due to the presence of an oestrogen receptor. A number of induced mammary tumours regress spontaneously, however, and the possiblity that these have lost the ability to concentrate oestrogen was investigated in the work described here.
Tumours were induced in female Sprague—Dawley (Wisconsin) rats by the gastric instillation of 20 mg. 7,12-DMBA (Sigma) at age 50 days. Rats with steadily growing tumours of approximately 2 cm. mean diameter were ovariectomized. Animals were used for uptake studies when tumours were clearly regressing, either spontaneously or in response to ovariectomy. Most of the latter were allowed to regress for 2–5 weeks but for comparison six tumours were used 4–8 days after ovariectomy. The rats were injected
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The use of androgens to cause the regression of mammary tumours in both rats and women is well established, but the mechanism by which they act is still obscure. Since it has been shown that some human breast tumours and oestrogen-responsive dimethylbenzanthracene (DMBA)-induced rat mammary tumours retain injected oestrogen, a possible mechanism for testosterone action might be the prevention of the concentration of oestrogen by the tumour tissue. Deshpande, Jensen, Bulbrook, Berne & Ellis (1967) had reported that pretreatment with dromostanolone propionate decreased the amount of injected [3H]oestradiol-17β present in human breast tumours compared with that in control patients, but this effect of androgen treatment has not been confirmed by Braunsberg, Carter, Irvine & James (1969). The effect of various testosterone treatments on the uptake of [6,7-3H]oestradiol by DMBA-induced mammary tumours of the rat is reported here.
Mammary tumours were induced in female Sprague—Dawley rats by the
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SUMMARY
The loss of injected tritiated oestradiol from the adrenals of non-tumour-bearing rats of different endocrine status and from the adrenals and tumours of animals bearing two lines of transplantable oestrone-induced adrenocortical carcinoma has been studied. There was no evidence that adrenals from non-tumour-bearing rats behaved as 'target organs' for oestrogen as regards retention of the hormone. As compared with skeletal muscle of the same animals, one tumour line and the host adrenals behaved in a similar way to normal adrenals and did not retain oestradiol, whereas the other tumour line and host adrenals lost the hormone at a somewhat slower rate than muscle.
It is suggested that the behaviour of the host adrenals and of the transplanted tumours regarding the injected oestrogen was determined more by the hormonal environment of the tissues including the contribution made by the tumour itself, than by specific oestrogen receptors in adrenal tissue.