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Introduction The involvement of estrogen in the development and progression of breast cancer is well known ( Henderson et al . 1988 , Helzlsouer & Couzi 1995 , Colditz 1998 , Keen & Davidson 2003 ). Most premenopausal and postmenopausal breast
Department of Pathobiology, College of Veterinary Medicine, Tuskegee University, Tuskegee, Alabama, USA
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Department of Veterinary Biosciences and Diagnostic Imaging, College of Veterinary Medicine, University of Georgia, Athens, Georgia, USA
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Department of Veterinary Biosciences and Diagnostic Imaging, College of Veterinary Medicine, University of Georgia, Athens, Georgia, USA
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Background Chronic exposure to low levels of estrogen is known to accelerate reproductive aging in female rats ( Kasturi et al. 2009 ). In fact, during the normal aging process, female rats go through a period of constant estrous when they
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concentrations. However, administration of pharmacologic doses of estrogen (17-β-estradiol, E 2 ) was known to augment the effect of thyroid hormone replacement to suppress TSHβ and CGA mRNA ( Wondisford 1996 and references therein). Indeed, E 2 inhibits
Group on Hormones and Signal Transduction, German Cancer Research Center, Heidelberg D-69120, Germany
Laboratory of Genomic Applications, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA
Department of Oncological Surgery, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
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Group on Hormones and Signal Transduction, German Cancer Research Center, Heidelberg D-69120, Germany
Laboratory of Genomic Applications, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA
Department of Oncological Surgery, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
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Group on Hormones and Signal Transduction, German Cancer Research Center, Heidelberg D-69120, Germany
Laboratory of Genomic Applications, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA
Department of Oncological Surgery, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
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Group on Hormones and Signal Transduction, German Cancer Research Center, Heidelberg D-69120, Germany
Laboratory of Genomic Applications, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA
Department of Oncological Surgery, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
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Group on Hormones and Signal Transduction, German Cancer Research Center, Heidelberg D-69120, Germany
Laboratory of Genomic Applications, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA
Department of Oncological Surgery, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
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Group on Hormones and Signal Transduction, German Cancer Research Center, Heidelberg D-69120, Germany
Laboratory of Genomic Applications, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA
Department of Oncological Surgery, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
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Group on Hormones and Signal Transduction, German Cancer Research Center, Heidelberg D-69120, Germany
Laboratory of Genomic Applications, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA
Department of Oncological Surgery, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
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indicating that the biological activity of the IGF system is strongly associated with estrogen status ( Lee et al. 1999 , Yee & Lee 2000 ). Estrogens were shown to increase IGF-I binding and IGF-IR mRNA levels in MCF-7 cells by sevenfold, suggesting that
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influencing these gender-related differences ( Walf & Frye 2005 , Scharfman & MacLusky 2008 , Stovall & Pinkentorn 2008 ). Estrogens have been found to modulate the functions of several physiological systems and their responses to stress in humans and
Faculty of Medicine, Center for Health Technology and Services Research (CINTESIS), University of Porto, Porto, Portugal
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division of the VMN (VMNvl) expresses estrogen receptor (ER) a and b and progesterone receptors (PRs), which depend on the levels of their cognate ligands ( Lauber et al . 1990 , Shughrue et al . 1992 , Sá et al . 2013 , 2015 ). Earlier studies have
Laboratory of Animal Physiology, Department of Animal Biology, Institute of Biomedical Technologies, University of La Laguna, La Laguna, Spain
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Laboratory of Animal Physiology, Department of Animal Biology, Institute of Biomedical Technologies, University of La Laguna, La Laguna, Spain
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Laboratory of Animal Physiology, Department of Animal Biology, Institute of Biomedical Technologies, University of La Laguna, La Laguna, Spain
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Laboratory of Animal Physiology, Department of Animal Biology, Institute of Biomedical Technologies, University of La Laguna, La Laguna, Spain
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Laboratory of Animal Physiology, Department of Animal Biology, Institute of Biomedical Technologies, University of La Laguna, La Laguna, Spain
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GnRH neuronal network to transynaptically modulate the final output of GnRH into the median eminence ( Herbison 1998 , Herbison & Pape 2001 ). Estradiol (E 2 ), the main endogenous regulator of the hypothalamus–pituitary axis, acts through estrogen
Department of Reproductive Biology, Mothers and Babies Research Centre, Department of Obstetrics and Gynaecology, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, Ohio 44106, USA
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Department of Reproductive Biology, Mothers and Babies Research Centre, Department of Obstetrics and Gynaecology, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, Ohio 44106, USA
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Introduction Estrogens (mainly estradiol (E 2 )) promote labor by stimulating biochemical and physical changes in myometrial cells that augment uterine contractility and excitability (for review, see Pepe & Albrecht (1995) ). Studies on various
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Introduction The hydroxysteroid (17-beta) dehydrogenase (HSD17B) enzymes catalyze the oxidoreduction of hydroxyl/keto groups of androgens and estrogens and regulate intracellular availability of steroid hormones ( Mindnich et al . 2004 ). To date
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cells. This upregulation is important for the anti-estrogenic effect of atRA ( Muller et al . 2002 ) and appears to affect the expression of the cell cycle regulator E2F-1. Forced expression of HES-1 inhibits an E 2 -mediated increase in E2F-1 and