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Department of Immunology, Manitoba Institute of Cell Biology, Department of Biochemistry and Medical Genetics, University of Manitoba, 471 Apotex Centre 750 McDermot Avenue, Winnipeg, Manitoba, Canada R3E 0T5
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Department of Immunology, Manitoba Institute of Cell Biology, Department of Biochemistry and Medical Genetics, University of Manitoba, 471 Apotex Centre 750 McDermot Avenue, Winnipeg, Manitoba, Canada R3E 0T5
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Department of Immunology, Manitoba Institute of Cell Biology, Department of Biochemistry and Medical Genetics, University of Manitoba, 471 Apotex Centre 750 McDermot Avenue, Winnipeg, Manitoba, Canada R3E 0T5
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Department of Immunology, Manitoba Institute of Cell Biology, Department of Biochemistry and Medical Genetics, University of Manitoba, 471 Apotex Centre 750 McDermot Avenue, Winnipeg, Manitoba, Canada R3E 0T5
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Department of Immunology, Manitoba Institute of Cell Biology, Department of Biochemistry and Medical Genetics, University of Manitoba, 471 Apotex Centre 750 McDermot Avenue, Winnipeg, Manitoba, Canada R3E 0T5
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Introduction Estrogen signaling through estrogen receptor α (ERα) is pivotal to the survival and maintenance of ERα + breast cancer tumors. Furthermore, the estrogen–ERα signaling axis has been shown to be indispensable to mammary gland development
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receptors which act as ligand-activated transcription factors. In women the key nuclear oestrogen receptors are ERα, encoded by ESR1 , and ERβ encoded by ESR2 : both receptors are expressed in endometrial tissue during the normal menstrual cycle
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Department of Gynecological Oncology, Department of Mathematics, Department of Clinical Biochemistry, Department of Molecular Bioenergetics, Academic Health Science Centre, Institute for Women's Health, Gynecological Cancer Research Centre, University College London, 149 Tottenham Road, London W1T 7DN, UK
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attractive alternative for breast cancer risk assessment. We found that estrogen receptor α (ERα) and ERβ serum bioactivity (SB) are independently associated with breast cancer using samples collected at diagnosis ( Widschwendter et al . 2009 ). To better
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Duke Proteomics and Metabolomics Resource, Duke University School of Medicine, Durham, NC, USA
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Clinical Trial Unit, Clinical Studies Sweden, Forum South, Skåne University Hospital, Lund, Sweden
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Background Obesity and hypercholesterolemia are associated with an increased risk of developing estrogen receptor-alpha (ERα)-positive breast cancers, especially among postmenopausal women ( Boyd & Mcguire 1990 , Bianchini et al . 2002
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endothelial cell migration and re-endothelialisation ( Umetani et al . 2007 ). In contrast, in the absence of E2, 27HC is reported to act as an agonist to ERα (ESR1) to increase cell adhesion and expression of pro-inflammatory cytokines such as tumour
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are recognized as co-mediators of tumor progression rather than as merely bystanders. Estrogen is well recognized as a mitogen for breast cancer cells. Traditionally, estrogenic effects have been ascribed to the nuclear estrogen receptors (ERα and ERβ
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Technologies) and transferred to nitrocellulose via an iBlot Transfer Stack and Blotting System (Life Technologies). Western blotting was performed with antibodies (diluted in 0.1% TBST at 1:1000 ratio) against the following: ERα (VP-E613, Vector Laboratories
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arms differed from each other regarding the expression of estrogen receptor alpha (ERα), ERβ and progesterone receptor (PgR) by Western blot. Briefly, 100 mg of frozen mammary tumor or endometrial tissue was ground using a mortar and pestle in liquid
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( Schwalbe et al . 2003 , Alarmo & Kallioniemi 2010 ). BMP-2 expression is significantly higher in the ER-negative tumours ( Julien et al . 2011 ). Silencing of ERα results in resistance to effects of oestradiol increased BMP-2 expression, and genetic
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), mineralocorticoid (MR, NR3C2), progesterone (PR, NR3C3), and androgen (AR, NR3C4) receptor ( Carson-Jurica et al. 1990 ). ERs are encoded by two different genes, ERα (NR3A1) and ERβ (NR3A2) ( Arnal et al. 2017 ). Unless specifically indicated, we will use the