Abstract
About one-third of human breast cancers require hormones for their continued growth1, and endocrine ablation or anti-hormone therapy can cause regression of these tumours. As a consequence, ovariectomy in premenopausal women or administration of an anti-oestrogen (tamoxifen) in postmenopausal women represent major options for treatment of metastatic breast cancer. Alternatively, chronic administration of agonistic analogues of luteinizing hormone-releasing hormone (LHRH)2 causes regression of mammary tumours in experimental animals3–6, and such treatment has shown promise in a small series of premenopausal women with advanced breast cancer7. It has been assumed that these results were achieved by suppressing the pituitary–ovarian axis, as the treatment causes a reduction in circulating levels of gonadal steroids similar to that produced by castration6–8. However, LHRH agonists can exert major effects on tissues other than the pituitary in animals9,10 and in the human11–15. Such findings, coupled with reports of LHRH in human breast milk16 and immunohistochemical evidence for the presence of LHRH-like activity in some human breast tumours17, prompted us to test whether LHRH agonists could have direct antitumour effects. We now report major direct effects of LHRH and its agonists on the growth of breast tumour cells in culture.
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Miller, W., Scott, W., Morris, R. et al. Growth of human breast cancer cells inhibited by a luteinizing hormone-releasing hormone agonist. Nature 313, 231–233 (1985). https://doi.org/10.1038/313231a0
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DOI: https://doi.org/10.1038/313231a0
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