Molecular mechanisms of estrogen carcinogenesis

James D Yager, J. G. Liehr

Research output: Contribution to journalArticle

Abstract

In western society, the causes of several cancers - including breast, endometrium, ovary, liver, and prostate - have been linked to inappropriate and/or prolonged exposure to synthetic or endogenous steroidal hormones. In this review, we discuss the mechanisms of estrogen carcinogenesis with a focus on estrogen metabolism to 16α-hydroxy estrone and 2- and 4-hydroxy catechol estrogens and the potential effects of these metabolites in vitro and in vivo on hamster liver and kidney and rat liver carcinogenesis models. The examples demonstrate that the parent compounds and their metabolites cause both nongenotoxic cell proliferative effects as well as direct and indirect genotoxic effects, which illustrates the complex nature of estrogen carcinogenesis. These effects, in combination with the metabolic state of the tissue and the timing of its exposure, may determine the cell type (organ) of tumor development and the severity of disease.

Original languageEnglish (US)
Pages (from-to)203-232
Number of pages30
JournalAnnual Review of Pharmacology and Toxicology
Volume36
StatePublished - 1996

Fingerprint

Liver
Estrogens
Carcinogenesis
Metabolites
Catechol Estrogens
Estrone
Metabolism
Rats
Tumors
Endometrium
Cricetinae
Hormones
Tissue
Prostate
Ovary
Breast Neoplasms
Kidney
Neoplasms

Keywords

  • catecholestrogens
  • estradiol
  • hepatocarcinogenesis
  • kidney carcinogenesis

ASJC Scopus subject areas

  • Pharmacology
  • Toxicology

Cite this

Molecular mechanisms of estrogen carcinogenesis. / Yager, James D; Liehr, J. G.

In: Annual Review of Pharmacology and Toxicology, Vol. 36, 1996, p. 203-232.

Research output: Contribution to journalArticle

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