Endocrine aspects of experimental renal carcinogenesis
Oestrogen has long been known to produce renal adenocarcinoma in the hamster. This hormone has also been suspected to be one of the aetiological factors in the human disease. However, it is not clear how oestrogen causes renal neoplasia. Study of the experimental tumour in the hamster has yielded some evidence incriminating the pituitary gland. Because of this, the role of the pituitary gland in the production of hamster renal adenocarcinoma has been investigated. A pharmacological method of suppressing hypophysial function, by reserpine-bromocriptine treatment, was developed for use in the hamster and was tested against tumour induction. The results showed that suppression of pituitary function reduced susceptability to tumour production in animals exposed to oestrogen. This supports the view that the pituitary gland is involved in renal carcinogenesis in this species. Of the many hypophysial secretions, the hormone prolactin was considered to be a culpable substance in renal tumorigenesis. This was supported by the finding that chronic hyperprolactinaemia, achieved by anterior lobe transplantation, enhanced the carcinogenic effect of oestrogen although it did not 'per se' cause tumours. On the contrary, hypoprolactinaemia, achieved by the administration of a prolactin-inhibitor (bromocriptine), decreased the neoplastic growth of renal tissue. It was concluded that the hormone prolactin may act like a promoter to oestrogen-induced renal adenocarcinoma in the hamster. It is possible that these findings may be relevant to the human disease. Therefore, it is recommended that investigation should be undertaken into the status of pituitary function in human renal adenocarcinoma. The results may advance our understanding of aetiological factors and may indicate new approaches to the control of this disease.