A Human Fetal Prostate Xenograft Model of Developmental Estrogenization

Prostate cancer is a common disease in older men. Rodent models have demonstrated that an early and later-life exposure to estrogen can lead to cancerous lesions and implicated hormonal dysregulation as an avenue for developing future prostate neoplasia. This study utilizes a human fetal prostate xe...

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Bibliographic Details
Published in:International journal of toxicology 2015-03, Vol.34 (2), p.119-128
Main Authors: Saffarini, Camelia M., McDonnell-Clark, Elizabeth V., Amin, Ali, Boekelheide, Kim
Format: Article
Language:English
Subjects:
Animals
Disease Models, Animal
Disease Progression
Estradiol - adverse effects
Estradiol - pharmacology
Gene Expression - drug effects
Heterografts - drug effects
Heterografts - embryology
Heterografts - pathology
Humans
Male
Prostate - drug effects
Prostate - embryology
Prostate - metabolism
Prostate - transplantation
Prostatic Hyperplasia - chemically induced
Prostatic Hyperplasia - etiology
Prostatic Hyperplasia - pathology
Prostatic Neoplasms - chemically induced
Prostatic Neoplasms - etiology
Prostatic Neoplasms - pathology
Rats, Nude
Testosterone - adverse effects
Testosterone - pharmacology
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Summary:Prostate cancer is a common disease in older men. Rodent models have demonstrated that an early and later-life exposure to estrogen can lead to cancerous lesions and implicated hormonal dysregulation as an avenue for developing future prostate neoplasia. This study utilizes a human fetal prostate xenograft model to study the role of estrogen in the progression of human disease. Histopathological lesions were assessed in 7-, 30-, 90-, 200-, and 400-day human prostate xenografts. Gene expression for cell cycle, tumor suppressors, and apoptosis-related genes (ie, CDKN1A, CASP9, ESR2, PTEN, and TP53) was performed for 200-day estrogen-treated xenografts. Glandular hyperplasia was observed in xenografts given both an initial and secondary exposure to estradiol in both 200- and 400-day xenografts. Persistent estrogenic effects were verified using immunohistochemical markers for cytokeratin 10, p63, and estrogen receptor α. This model provides data on the histopathological state of the human prostate following estrogenic treatment, which can be utilized in understanding the complicated pathology associated with prostatic disease and early and later-life estrogenic exposures.
ISSN:1091-5818
1092-874X
DOI:10.1177/1091581815569364