Abstract
Aminoglutethimide without glucocorticoid has been shown to be a clinically effective treatment for postmenopausal breast cancer in low dosage (250 mg day-1). The mechanism of action of this approach is thought to be the inhibition of peripheral aromatase, the enzyme which converts androstenedione to oestrone. The activity of this enzyme was measured in vivo by injection with 3H-androstenedione and 14C-oestrone and found to be 0.20% +/- 0.05 in 5 patients on low dose AG therapy. In comparison with previously published data this demonstrates a 92% inhibition of peripheral aromatase activity confirming aromatase inhibition as a viable aim in the endocrine treatment of breast cancer.
Highlights
Aminoglutethimide without glucocorticoid has been shown to be a clinically effective treatment for postmenopausal breast cancer in low dosage (250mgday-1)
Aminoglutethimide (AG) is a clinically effective endocrine treatment for advanced postmenopausal breast cancer (Lipton et al, 1974; Smith et al, 1978; Santen et al, 1981; Harris et al, 1982), in which it has been used almost exclusively in doses of 750-1000mgday-1, in combination with hydrocortisone (HC). This therapeutic regime was derived with the aim of suppressing adrenal androgen synthesis (Lipton et al, 1974; Wells et al, 1978) which was expected to result from previously reported inhibition by AG of the conversion of cholesterol to pregnenolone by 20,22-desmolase (Cohen, 1967; Dexter et al, 1967)
We report here the measurement of this activity in vivo in postmenopausal breast cancer patients undergoing treatment at a lower dosage (250mg day 1)
Summary
Aminoglutethimide without glucocorticoid has been shown to be a clinically effective treatment for postmenopausal breast cancer in low dosage (250mgday-1). Aminoglutethimide (AG) is a clinically effective endocrine treatment for advanced postmenopausal breast cancer (Lipton et al, 1974; Smith et al, 1978; Santen et al, 1981; Harris et al, 1982), in which it has been used almost exclusively in doses of 750-1000mgday-1, in combination with hydrocortisone (HC) This therapeutic regime was derived with the aim of suppressing adrenal androgen synthesis (Lipton et al, 1974; Wells et al, 1978) which was expected to result from previously reported inhibition by AG of the conversion of cholesterol to pregnenolone by 20,22-desmolase (Cohen, 1967; Dexter et al, 1967). 1979) and this has led to the examination of the clinical and endocrine effectiveness of AG at low dosage (250mgday-1)
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