EFFECT OF DIETHYLSTILBESTROL-INDUCED TUMORIGENESIS ON THE SECRETORY ACTIVITY OF THE RAT ANTERIOR PITUITARY GLAND1

Abstract

The secretion of prolactin is stimulated by chronic estrogen administration. This hormone is maintained approximately at normal concentration in the rapidly proliferating tumor tissue. The secretion of adrenocorticotropin occurs at an accelerated rate during the chronic administration of diethyl-stilbestrol, and is not modified markedly by tumorous pituitary growth. Compensatory thyroid hypertrophy occurs at almost the same rate in tumor-bearing and control animals. Secretion and storage of both follicle-stimulating and luteinizing hormones is inhibited during diethylstilbestrol administration. Tibial line assays suggest that the growth hormone concentration in tumor tissue is less than in normal pituitary tissue. It is suggested that pituitary tumorigenesis is the result of the continual and prolonged maintenance of a normal mitotic response to estrogen in the prolactin-producing cells. The cells which produce the other pituitary hormones do not seem to be involved in the tumorigenic process.