Direct Effects of LHRH and Agonists on Human Breast Cancer Cells

Abstract

The growth of the human female breast is clearly under endocrine control. In the absence of stimulatory hormones, the breast remains rudimentary whilst major development normally only occurs at times of increased hormone production such as puberty and pregnancy. It is, therefore, not surprising that certain breast cancers should also require hormones for their continued growth. Whilst polypeptide hormones are capable of influencing events within breast cancers, (Dilley and Kister, 1975, Leung and Shiu, 1981) the most convincing evidence for the involvement of endocrine agents is for steroid hormones, particularly oestrogens. This includes the observations that, a) the growth of cell lines of human breast cancer may be stimulated by oestrogen both in culture (Butler et al, 1981, Benz et al, 1983) and in immunosuppressed animals (Shafie 1980, Seibert et al, 1983); b) the administration of oestrogen to breast cancer patients with metastatic deposits in bone may cause increased urinary calcium excretion due to accelerated tumour growth (Pearson et al, 1954); c) oestrogen deprivation therapy causes regression of breast cancers in about one-third of patients with advanced disease (Henderson and Canellos, 1980); d) these effects are invariably associated with tumours which possess receptors for oestrogen (Jensen et al, 1974, McGuire et al, 1975). Endocrine intervention therefore represents a major treatment option for advanced breast cancer especially against tumours which are rich in oestrogen receptors.