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Pratima Basak 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
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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Sumanta Chatterjee 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
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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Steven Weger 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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M Christine Bruce 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
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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Leigh C Murphy 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
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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Afshin Raouf 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
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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Eva Baxter Department of Cell and Molecular Biology, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia

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Karolina Windloch Department of Cell and Molecular Biology, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia

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Greg Kelly Department of Cell and Molecular Biology, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia

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Jason S Lee Department of Cell and Molecular Biology, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia

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Frank Gannon Department of Cell and Molecular Biology, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia

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Donal J Brennan UCD School of Medicine, Catherine McAuley Research Centre, Mater Misericordiae University Hospital, Dublin, Ireland
Cancer Biology and Therapeutics Laboratory, UCD Conway Institute of Biomolecular and Biomedical Science, University College Dublin, Belfield, Dublin, Ireland
Systems Biology Ireland, University College Dublin, Belfield, Dublin, Ireland

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( Carlson et al. 2014 ). Tamoxifen is a selective oestrogen receptor modulator, acting as an oestrogen receptor alpha (ERα) antagonist in the breast and as an agonist in the endometrium, increasing the risk of developing endometrial cancer ( Cohen 2004

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Hiroko Yamashita
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Mariko Nishio
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Tatsuya Toyama
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Hiroshi Sugiura
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Naoto Kondo
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Shunzo Kobayashi
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Yoshitaka Fujii
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Hirotaka Iwase Oncology, Breast and Endocrine Surgery, Immunology and Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-ku, Nagoya 467-8601, Japan

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, Ellis 2004 ). ERα is phosphorylated on multiple amino acid residues ( Lannigan 2003 ). In general, phosphorylation of serine residues in the activation function 1 (AF-1) domain of ERα appears to influence the recruitment of coactivators, resulting in

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Clarissa Wormsbaecher Department of Molecular Genetics, The Ohio State University, Columbus, Ohio, USA
The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, USA

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Brittney M Cumbia The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, USA

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Emma G Amurgis The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, USA

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Jillian M Poska Department of Molecular Genetics, The Ohio State University, Columbus, Ohio, USA
The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, USA

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Madeline R Price Department of Molecular Genetics, The Ohio State University, Columbus, Ohio, USA
The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, USA

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Xiaokui M Mo Department of Biomedical Informatics, Center for Biostatistics, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA

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Sue E Knoblaugh Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio, USA

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Takeshi Kurita The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, USA
Department of Cancer Biology and Genetics, The Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, USA

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Craig Joseph Burd Department of Molecular Genetics, The Ohio State University, Columbus, Ohio, USA
The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, USA

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Introduction Estrogen receptor alpha (ERα) is required for full mammary gland development. ERα-knockout mice have mammary glands that appear normal at birth but fail to mature. Specifically, adult ERα-knockout mice have a primitive ductal

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Barbara Kuske
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Catherine Naughton
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Kate Moore
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Kenneth G MacLeod
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William R Miller
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Robert Clarke
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Simon P Langdon
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David A Cameron
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Introduction Estrogen receptor α (ERα) is a major growth regulator for many breast cancers and has provided an exploitable target for therapy ( Ali & Coombes 2002 ). Estrogen binding to ERα promotes conformational changes in the

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Yuanzhong Wang Department of Cancer Biology, Beckman Research Institute of the City of Hope, Duarte, California, USA

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Yen-Dun Tony Tzeng Department of Cancer Biology, Beckman Research Institute of the City of Hope, Duarte, California, USA
Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung City, Taiwan, Republic of China

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Gregory Chang Department of Cancer Biology, Beckman Research Institute of the City of Hope, Duarte, California, USA

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Xiaoqiang Wang Department of Cancer Biology, Beckman Research Institute of the City of Hope, Duarte, California, USA

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Shiuan Chen Department of Cancer Biology, Beckman Research Institute of the City of Hope, Duarte, California, USA

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the two most common endocrine treatments of ER+ breast cancer. Tamoxifen antagonizes the binding of estrogen to ERα, while AIs block estrogen biosynthesis by inhibition of aromatase, the key enzyme that converts androgens into estrogens. Clinical

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N Sarwar
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J-S Kim
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J Jiang
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D Peston
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H D Sinnett
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P Madden
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J M Gee
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R I Nicholson
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A E Lykkesfeldt
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S Shousha
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R C Coombes
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S Ali
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Introduction It is now clear that oestrogens play a central role in promoting breast cancer development and progression ( Ali & Coombes 2002 ). In this respect, oestrogen action is mediated through the oestrogen receptors ERα and ERβ

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Corinne N Haines Department of Molecular Genetics, The Ohio State University, Columbus, Ohio, USA
The Ohio State University, Comprehensive Cancer Center, Columbus, Ohio, USA

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Kara M Braunreiter Department of Molecular Genetics, The Ohio State University, Columbus, Ohio, USA

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Xiaokui Molly Mo Center for Biostatistics, The Ohio State University, Wexner Medical Center, Columbus, Ohio, USA

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Craig J Burd Department of Molecular Genetics, The Ohio State University, Columbus, Ohio, USA
The Ohio State University, Comprehensive Cancer Center, Columbus, Ohio, USA

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-dependent breast cancer, the activation of ERα ultimately leads to proliferation ( Dixon 2014 ). ER-positive breast cancers are treated with endocrine therapies that disrupt the activity of ERα ( Heldring et al . 2007 ). Unfortunately, patients develop resistance

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Philip Jonsson Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, 3605 Cullen Blvd., Houston, Texas 77204-5056, USA

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Anne Katchy Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, 3605 Cullen Blvd., Houston, Texas 77204-5056, USA

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Cecilia Williams Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, 3605 Cullen Blvd., Houston, Texas 77204-5056, USA

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Introduction The role of estrogen receptor α (ERα ( ESR1 )) as a biological marker and target in breast cancer therapy is clear. ERα antagonists, such as tamoxifen, or estrogen ablation using aromatase inhibitors are efficient therapeutic approaches

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Sarah A Dabydeen Departments of Oncology, Medicine, Lombardi Comprehensive Cancer Center, Georgetown University, 3970 Reservoir Road NW, Research Building, Room 520A, Washington, District of Columbia 20057, USA

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Priscilla A Furth Departments of Oncology, Medicine, Lombardi Comprehensive Cancer Center, Georgetown University, 3970 Reservoir Road NW, Research Building, Room 520A, Washington, District of Columbia 20057, USA
Departments of Oncology, Medicine, Lombardi Comprehensive Cancer Center, Georgetown University, 3970 Reservoir Road NW, Research Building, Room 520A, Washington, District of Columbia 20057, USA

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Introduction Breast cancer is a heterogeneous disease consisting of four clinically relevant categories based on the expression patterns of estrogen receptor α (ERα; ESR1 ) and V-Erb-B2 avian erythroblastic leukemia viral oncogene homolog 2 ( HER2

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