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changing demographics characterized by an aging population and increased prevalence of obesity ( Sanderson et al. 2017 ). Clinically, endometrial cancers are routinely classified as having a type I or type II phenotype, with the former being oestrogen
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). Adjuvant endocrine therapy for early breast cancer patients became widespread in the mid to late 1980s ( Davies et al . 2013 ). Two main categories of drugs target the dependence of malignant breast epithelial cells upon oestrogens. Aromatase inhibitors
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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
The Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, UK
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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
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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breast cancers ( Cancer Research UK 2017 ). Even for those treated at an early stage, there is still a significant risk of relapse, often several years later. This is particularly true of oestrogen receptor-positive breast cancers, which are at a
Division of Environmental Genetics and Molecular Toxicology, Division of Epidemiology and Biostatistics, Center for Environmental Genetics, Cancer Center, Department of Pathology, Department of Pathology and Laboratory Medicine, Department of Environmental Health
Division of Environmental Genetics and Molecular Toxicology, Division of Epidemiology and Biostatistics, Center for Environmental Genetics, Cancer Center, Department of Pathology, Department of Pathology and Laboratory Medicine, Department of Environmental Health
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Division of Environmental Genetics and Molecular Toxicology, Division of Epidemiology and Biostatistics, Center for Environmental Genetics, Cancer Center, Department of Pathology, Department of Pathology and Laboratory Medicine, Department of Environmental Health
Division of Environmental Genetics and Molecular Toxicology, Division of Epidemiology and Biostatistics, Center for Environmental Genetics, Cancer Center, Department of Pathology, Department of Pathology and Laboratory Medicine, Department of Environmental Health
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. Henderson BE Bernstein L Ross RK Depue RH Judd HL 1988 The early in utero oestrogen and testosterone environment of blacks and whites: potential effects on male offspring . British Journal of Cancer 57 216 – 218 . Ho SM Leung YK
Cancer Biology Laboratory, The Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia
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St. Vincent’s Clinical School, Faculty of Medicine, University of New South Wales Australia, Sydney, New South Wales, Australia
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). These processes are tightly controlled by hormones. Oestrogens, progesterone and prolactin act on the mammary epithelium in synergy with corticosteroids and growth hormone to orchestrate mammary gland development ( Brisken & O’Malley 2010 , Macias
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), presumably enabling androgen-stimulated cell cycle entry and growth. More recently, PHB has been shown to be a corepressor of the oestrogen receptor (ERα; He et al . 2008 ), associating with oestrogen-regulated promoters in the absence of hormone and
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Society with Dr Jordan’s selection as the 2018 Endocrine Society Laureate of the Gerald D Aurbach Award for Outstanding Translational Research. References Abderrahman B Jordan VC 2016 Improving long-term adjuvant anti-oestrogenic therapy