Principles of endocrine therapy

It has long been known that oestrogen is capable of stimulating the growth of breast and endometrial cancers, and androgens the growth of prostate cancer. Removal of these growth factors by manipulation of the hormonal environment may result in apoptosis and regression of the cancer. Endocrine therapy can be curative in a proportion of patients treated for micrometastatic disease in the adjuvant setting for breast and prostate cancer and provides a minimally toxic non-curative (palliative) treatment in advanced/metastatic disease. The presence of detectable cellular receptors for the hormone markedly increases the likelihood that the therapy will be effective. The binding of hormone to receptor and translocation of the hormone-receptor complex into the nucleus, where it binds to specific hormone-responsive transcription factors on the DNA.

About one-third of patients with breast cancer have receptors for oestrogens and progesterones. Hormonal manipulation includes the use of tamoxifen, which blocks oestrogen receptors, and the reduction of endogenous oestrogen by oophorectomy or 'medical oophorectomy' via pituitary downregulation using a gonadotrophin-releasing hormone (GnRH) analogue such as goserilin. In patients with advanced metastatic breast cancer, oestrogen deprivation causes tumour regression in 30% of unselected women and in more than 60% of those with oestrogen-receptor-positive tumours for a median duration of 20 months.

Progestogens have a direct effect in breast tumour cells as well as effects on the pituitary/ovarian and adrenal axis and can be as effective as tamoxifen. In postmenopausal women, androgens are synthesized by the adrenal glands and converted in subcutaneous fat to estrone by the enzyme aromatase. Aromatase inhibitors, for example anastrozole, reduce circulating oestrogen levels and oestrogen synthesis in tumour cells and have recently shown even greater efficacy than tamoxifen in the treatment of metastatic breast cancer in the postmenopausal woman.

Endometrial cancers have receptors for both oestrogens and progestogens. Approximately 20% of receptor-positive metastases will regress for a median 20 months with synthetic progestogens such as medroxyprogesterone acetate but paradoxically tamoxifen has little effect. Trials to date with adjuvant progestogens have not been successful in increasing survival.

In advanced prostate cancer, androgen deprivation induces regression in 70% of cases for a median duration of 24 months. GnRH agonists, e.g. goserilin, and orchidectomy, are equally effective; however, androgen receptor blockers such as flutamide are less so. Combinations of goserilin and flutamide may be used in the initial phase of treatment to avoid a disease flare from the initial agonist action of GnRH analogues, but prolonged combination therapy has been no more effective than goserilin alone. In the adjuvant setting, the addition of androgen deprivation to prostatic radiotherapy or surgery has improved survival and continues to be investigated.

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