A new understanding of the hormonal regulation of endocrine dependent cancer.
In the last decade there have been major developments in our understanding of the hormonal control of cancer. The steroid receptor has been characterized and its gene cloned. Peptide hormone receptors and their ligands have been identified within the cancer cell providing supporting evidence for the significance of the autocrine hypothesis in the regulation of cell growth. Conventional wisdom describes different levels at which hormonal therapies for endocrine related malignancies operate, regulating cell growth by decreasing levels of circulating sex steroids upon which the cell depends. Current theories incorporate this hypothesis into a different schemata where there are two levels of control of cell growth. The paracrine hypothesis describes a situation where tumours are dependent upon the secretion of a distant factor for their growth and this is exemplified by the dependence of some breast tumours upon oestrogenic steroids. An alternative scenario involves the regulation of tumours by locally secreted growth factors and this is the autocrine hypothesis, examples of which may include transforming growth factors and gonadotrophin releasing hormone like factors in breast and prostatic cancer. This article describes the role of paracrine and autocrine factors in the control of hormone dependent malignancy.
Waxman
J
J
Department of Clinical Oncology, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
D005260:Female; D006728:Hormones / Q000502:physiology*; D006801:Humans; D008297:Male; D009376:Neoplasms, Hormone-Dependent / Q000503:physiopathology* / Q000628:therapy; D011956:Receptors, Cell Surface
D006728:Hormones; D011956:Receptors, Cell Surface