ESTROGEN-INDUCED TUMORIGENESIS IN THE COPENHAGEN RAT - DISPARATE SUSCEPTIBILITIES TO DEVELOPMENT OF PROLACTIN-PRODUCING PITUITARY-TUMORS AND MAMMARY CARCINOMAS
Tj. Spady et al., ESTROGEN-INDUCED TUMORIGENESIS IN THE COPENHAGEN RAT - DISPARATE SUSCEPTIBILITIES TO DEVELOPMENT OF PROLACTIN-PRODUCING PITUITARY-TUMORS AND MAMMARY CARCINOMAS, Cancer letters, 124(1), 1998, pp. 95-103
The Copenhagen (COP) rat is unique among inbred rat strains in its hig
h degree of resistance to spontaneously arising and induced mammary ca
ncers. Hyperprolactinemia resulting from tumors of the anterior pituit
ary gland has been suggested to be the causative factor in the etiolog
y of estrogen-induced mammary cancer in rats. Therefore, we have exami
ned the ability of administered estrogens to induce development of PRL
-producing pituitary tumors and mammary carcinomas in COP rats. Diethy
lstilbestrol (DES), administered to male COP rats for 12 weeks, beginn
ing when the animals were 9 weeks of age, induced development of PRL-p
roducing pituitary tumors, defined as grossly enlarged pituitary masse
s displaying lactotroph hyperplasia and associated hyperprolactinemia.
When treated with 17 beta-estradiol (E2), female COP rats developed p
ituitary tumors and hyperprolactinemia, but displayed a high degree of
resistance to development of mammary carcinomas. These data indicate
that E2-induced hyperprolactinemia is insufficient to induce developme
nt of mammary carcinomas in the female COP rat. (C) 1998 Elsevier Scie
nce Ireland Ltd.