Developmental estrogenization and prostatic neoplasia

Authors

  • Risto Santti,

    1. Institute of Biomedicine, Department of Anatomy, University of Turku, Turku, Finland
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  • Sari Mäkelä,

    1. Institute of Biomedicine, Department of Anatomy, University of Turku, Turku, Finland
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  • Liisa Pylkkänen,

    1. Institute of Biomedicine, Department of Anatomy, University of Turku, Turku, Finland
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  • Retha R. Newbold,

    Corresponding author
    1. Developmental Endocrinology and Pharmacology Section, Laboratory of Reproductive and Developmental Toxicology, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina
    • Developmental Endocrinology and Pharmacology Section, Laboratory of Reproductive and Developmental Toxicology, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709
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  • John A. McLachlan

    1. Developmental Endocrinology and Pharmacology Section, Laboratory of Reproductive and Developmental Toxicology, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina
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Abstract

The association of estrogens with benign prostatic hyperplasia and prostatic cancer has been widely studied, but no conclusive evidence exists for a role of estrogens in prostatic disease. This paper reviews the literature and describes studies which have sought to show a correlation of estrogens and alterations in the prostates of humans and experimental animal models. Using the developmentally estrogenized mouse model, we propose an alternative role for estrogens as a predisposing factor for prostatic diseases: estrogen exposure during development may initiate cellular changes in the prostate which would require estrogens and/or androgens later in life for promotion to hyperplasia or neoplasia. Thus, the critical time for estrogen action would be during the development of the prostatic tissue. We further suggest that estrogen-sensitive cells may remain in the prostate and be more responsive to estrogens later in life or less responsive to the normal controlling mechanisms of prostatic growth. © 1994 Wiley-Liss, Inc.

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