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Estrogen receptors and human disease: an update

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Abstract

A myriad of physiological processes in mammals are influenced by estrogens and the estrogen receptors (ERs), ERα and ERβ. As we reviewed previously, given the widespread role for estrogen in normal human physiology, it is not surprising that estrogen is implicated in the development or progression of a number of diseases. In this review, we are giving a 5-year update of the literature regarding the influence of estrogens on a number of human cancers (breast, ovarian, colorectal, prostate, and endometrial), endometriosis, fibroids, and cardiovascular disease. A large number of sophisticated experimental studies have provided insights into human disease, but for this review, the literature citations were limited to articles published after our previous review (Deroo and Korach in J Clin Invest 116(3):561–570, 2006) and will focus in most cases on human data and clinical trials. We will describe the influence in which estrogen’s action, through one of or both of the ERs, mediates the aforementioned human disease states.

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Abbreviations

ER:

Estrogen receptor

PR:

Progesterone receptor

AR:

Androgen receptor

DPN:

Diarylpropionitrile

MAPK:

Mitogen-activated protein kinase

HER2:

Human epidermal growth factor receptor 2

UTR:

Untranslated region

SNP:

Single-nucleotide polymorphism

miRNA:

MicroRNA

FOX:

Forkhead binding protein

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Acknowledgments

This research was supported by Z01ES70065 to KSK by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences.

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The authors have declared that no conflict of interest exists.

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Correspondence to Kenneth S. Korach.

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Burns, K.A., Korach, K.S. Estrogen receptors and human disease: an update. Arch Toxicol 86, 1491–1504 (2012). https://doi.org/10.1007/s00204-012-0868-5

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