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Douglas A Gibson Medical Research Council Centre for Inflammation Research, The University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Frances Collins Medical Research Council Centre for Inflammation Research, The University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Fiona L Cousins Medical Research Council Centre for Inflammation Research, The University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Arantza Esnal Zufiaurre Medical Research Council Centre for Inflammation Research, The University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Philippa T K Saunders Medical Research Council Centre for Inflammation Research, The University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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agonists on the endometrium or endometrial malignancies is not known. In addition to activating LXRs, 27HC can also bind oestrogen receptors (ER) ( Umetani et al . 2007 ) and acts as an endogenous selective oestrogen receptor modulator (SERM) ( DuSell

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S C J P Gielen
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L C M Kühne
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P C Ewing
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L J Blok
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C W Burger
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Introduction Tamoxifen is the first-choice adjuvant treatment for primary oestrogen receptor-positive (ER+) breast cancer in postmenopausal women. It has been shown that survival rates in tamoxifen-treated women are improved as much

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Anastasia Alataki Ralph Lauren Centre for Breast Cancer Research, Royal Marsden Hospital and The Institute of Cancer Research, London, UK
The Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, UK

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Mitch Dowsett Ralph Lauren Centre for Breast Cancer Research, Royal Marsden Hospital and The Institute of Cancer Research, London, UK
The Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, UK

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Introduction Breast cancer development and progression are significantly affected by signalling pathways involving oestrogen receptor (ER) and growth factor receptors ( Arpino et al. 2008 ). Over 80% of all breast cancer cases are deemed ER

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Abigail Read The Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, UK
Division of Molecular Pathology, The Institute of Cancer Research, London, UK

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Rachael Natrajan The Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, UK
Division of Molecular Pathology, The Institute of Cancer Research, London, UK

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examples of common driver oncogenes and tumour suppressor genes that can be aberrantly spliced in breast cancer. AS has also been shown to regulate protein diversity of the oestrogen receptor itself. In particular, previous studies have shown the ERαΔ5

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Gerard A Tarulli Dame Roma Mitchell Cancer Research Laboratories (DRMCRL) Faculty of Health Sciences, School of Medicine, The University of Adelaide, Adelaide, South Australia 5005, Australia

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Lisa M Butler Dame Roma Mitchell Cancer Research Laboratories (DRMCRL) Faculty of Health Sciences, School of Medicine, The University of Adelaide, Adelaide, South Australia 5005, Australia

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Wayne D Tilley Dame Roma Mitchell Cancer Research Laboratories (DRMCRL) Faculty of Health Sciences, School of Medicine, The University of Adelaide, Adelaide, South Australia 5005, Australia

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Theresa E Hickey Dame Roma Mitchell Cancer Research Laboratories (DRMCRL) Faculty of Health Sciences, School of Medicine, The University of Adelaide, Adelaide, South Australia 5005, Australia

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Introduction Development of the adult mammary gland and its function are dependent upon oestrogen and progesterone acting via the oestrogen receptor alpha (ERa (ESR1)) and progesterone receptor (PR (PGR)) respectively. During reproductive cycles

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S C Drury Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK
Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK

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S Detre Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK

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A Leary Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK

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J Salter Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK
Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK

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J Reis-Filho Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK

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V Barbashina Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK

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C Marchio Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK

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E Lopez-Knowles Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK

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Z Ghazoui Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK

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K Habben Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK

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S Arbogast Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK

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S Johnston Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK

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M Dowsett Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK
Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK

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Introduction Until recently, tamoxifen has been the gold standard endocrine treatment for oestrogen receptor-positive (ER+) breast cancer and despite the advent of aromatase inhibitors, it continues to be an important therapeutic option. Tamoxifen

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Nicoletta Biglia Academic Department of Gynaecological Oncology, Mauriziano Umberto I° Hospital of Turin and Institute for Cancer Research and Treatment of Candiolo, University of Turin, Largo Turati 62, 10129 Turin, Italy

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Luca Mariani Academic Department of Gynaecological Oncology, Mauriziano Umberto I° Hospital of Turin and Institute for Cancer Research and Treatment of Candiolo, University of Turin, Largo Turati 62, 10129 Turin, Italy

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Luca Sgro Academic Department of Gynaecological Oncology, Mauriziano Umberto I° Hospital of Turin and Institute for Cancer Research and Treatment of Candiolo, University of Turin, Largo Turati 62, 10129 Turin, Italy

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Paola Mininanni Academic Department of Gynaecological Oncology, Mauriziano Umberto I° Hospital of Turin and Institute for Cancer Research and Treatment of Candiolo, University of Turin, Largo Turati 62, 10129 Turin, Italy

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Giulia Moggio Academic Department of Gynaecological Oncology, Mauriziano Umberto I° Hospital of Turin and Institute for Cancer Research and Treatment of Candiolo, University of Turin, Largo Turati 62, 10129 Turin, Italy

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Piero Sismondi Academic Department of Gynaecological Oncology, Mauriziano Umberto I° Hospital of Turin and Institute for Cancer Research and Treatment of Candiolo, University of Turin, Largo Turati 62, 10129 Turin, Italy

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cancer risk of oestrogen plus progestin associations as compared with oestrogen alone (ERT; Colditz et al. 1995 , Persson et al. 1996 , Colditz & Rosner 1998 , Magnusson et al. 2000 , Ross et al. 2000 , Schairer et al. 2000 , Rossouw et

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Eva Hadadi Myeloid Cell Immunology Lab, VIB Center for Inflammation Research, Brussels, Belgium
Lab of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium

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Hervé Acloque INSERM U935, University Paris Saclay, Villejuif, Ile-de-France, France
Université Paris-Saclay, INRAE, AgroParisTech, GABI, Jouy-en-Josas, Ile-de-France, France

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-inflammatory, anti-oxidative, anti-angiogenic, anti-proliferative and pro-apoptotic properties (reviewed in Hill et al. 2015 ). Melatonin is also able to disrupt oestrogen-dependent cell signalling and has also been shown to slow down EMT induction in breast

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P L Jeffery Ghrelin Research Group, Hormone-dependent Cancer Programme, School of Life Sciences, Queensland University of Technology, PO Box 2434, Brisbane 4001, Australia

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R E Murray Ghrelin Research Group, Hormone-dependent Cancer Programme, School of Life Sciences, Queensland University of Technology, PO Box 2434, Brisbane 4001, Australia

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A H Yeh Ghrelin Research Group, Hormone-dependent Cancer Programme, School of Life Sciences, Queensland University of Technology, PO Box 2434, Brisbane 4001, Australia

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J F McNamara Ghrelin Research Group, Hormone-dependent Cancer Programme, School of Life Sciences, Queensland University of Technology, PO Box 2434, Brisbane 4001, Australia

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R P Duncan Ghrelin Research Group, Hormone-dependent Cancer Programme, School of Life Sciences, Queensland University of Technology, PO Box 2434, Brisbane 4001, Australia

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G D Francis Ghrelin Research Group, Hormone-dependent Cancer Programme, School of Life Sciences, Queensland University of Technology, PO Box 2434, Brisbane 4001, Australia

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A C Herington Ghrelin Research Group, Hormone-dependent Cancer Programme, School of Life Sciences, Queensland University of Technology, PO Box 2434, Brisbane 4001, Australia

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L K Chopin Ghrelin Research Group, Hormone-dependent Cancer Programme, School of Life Sciences, Queensland University of Technology, PO Box 2434, Brisbane 4001, Australia

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autocrine/paracrine pathway exists to promote cell growth in breast cancer, as appears to be the case in prostate cancer ( Jeffery et al. 2002 ). Materials and methods Cell culture Oestrogen-dependent breast cancer

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S Zanardi
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D Serrano
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A Argusti
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M Barile
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M Puntoni
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A Decensi
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Introduction Despite recent progress in treatment and therapeutic strategies, breast cancer incidence, morbidity and mortality remain a major problem in Western countries. Recent trials with selective oestrogen receptor modulators

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