Carcinogenesis, Vol 19, 2173-2180, Copyright © 1998 by Oxford University Press
DZ Liao, CG Pantazis, X Hou and SA Li
Both endogenous and exogenous estrogen exposure is associated with an
increased breast cancer risk. In some studies, elevated serum testosterone
levels have also been linked to an increased breast cancer risk. Estrogen
alone or combined with progesterone induces high mammary tumor incidences
in various strains of both male and female rats. Mammary gland ductal
adenocarcinomas were induced after 17beta- estradiol (E2) and testosterone
propionate (TP) treatment in male Noble rats. Tumor incidence was 100%
after 8-9 months of treatment. Such neoplasms were not detected after
either estrogen or androgen exposure alone within this time period. TP
alone caused disruption of mammary gland ducts and proliferation of stromal
tissue, while E2 treatment alone induced both ductal epithelial growth and
nodular atypical hyperplasia. To study the interaction of these hormones in
mammary tumorigenesis, sex hormone receptors were characterized in mammary
glands of Noble rats. Estrogen receptor-alpha (ER) was detected in age-
matched, untreated mammary gland epithelium; in most early atypical
hyperplastic lesions appearing after E2 and E2 + TP treatment and in E2 +
TP-induced mammary tumors. Two major ER putative isoforms, 116 and 120 kDa,
were detected in E2- and E2 + TP-treated mammary glands, and in the induced
tumors. A 54 kDa ER protein was found in untreated and TP-treated mammary
glands, and in the induced tumors. Both progesterone receptor-B (PR-B) and
PR-A2, as well as androgen receptor-B (AR-B) and AR-A isoforms were
markedly elevated in all E2 + TP-induced mammary tumors. However, the
levels of both PR and AR were very low in mammary glands of E2- and E2 +
TP-treated male rats. Low and moderate levels of AR and PR, respectively,
were detected in most atypical hyperplastic lesions induced by E2- and E2 +
TP-treated mammary glands. These results suggest that androgens may
interact with either AR or PR, and perhaps both receptors, in E2 +
TP-induced mammary glands and the induced tumors to effect the reduction in
latency period, enhance tumor size, and increase incidence to 100%.
ARTICLES
Promotion of estrogen-induced mammary gland carcinogenesis by androgen in the male Noble rat: probable mediation by steroid receptors
Hormonal Carcinogenesis Laboratory, Division of Etiology and Prevention of Hormonal Cancers, Kansas Cancer Institute, University of Kansas Medical Center, Kansas City 66160-7312, USA.
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