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Consortium for the Study of Thyroid Cancer (CECaT), Catalonia, Spain
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Program of Predictive and Personalized Medicine of Cancer, Germans Trias i Pujol Research Institute (PMPPC-IGTP), Barcelona, Spain
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Introduction Thyroid cancer, the most prevalent endocrine malignancy, covers the full range of phenotypes from indolent to the worst forms of human cancer. It is categorized into differentiated thyroid cancer (DTC), poorly differentiated
Shanghai Jiao Tong University School of Medicine, Shanghai, China
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Introduction Thyroid cancer is the fifth most common cancer in women in the United States and is the most commonly diagnosed cancer before the age of 30 years among women in China ( Chen et al. 2016 ). Although thyroid cancer is generally
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thyroid carcinoma. With globally rising incidence, thyroid carcinoma has attracted much more concern than before. In theory, thyrotoxicosis with suppressed TSH should lead to a lower incidence of thyroid cancer than that observed in euthyroid patients
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Introduction Thyroid cancer is the most common cancer of endocrine system, with a rapid worldwide increase over recent decades ( Enewold et al. 2009 , Kilfoy et al. 2009 , Chen et al. 2016 ). The disease is classified into three types
School of Medicine and Public Health, University of Newcastle, Newcastle, Australia
Hunter Medical Research Institute, Newcastle, New South Wales, Australia
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Hunter Medical Research Institute, Newcastle, New South Wales, Australia
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Department of Medical Oncology, Calvary Mater Newcastle, Waratah, Australia
School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, Australia
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Hunter Medical Research Institute, Newcastle, New South Wales, Australia
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Department of Surgery, John Hunter Hospital, Newcastle, Australia
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School of Medicine and Public Health, University of Newcastle, Newcastle, Australia
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School of Medicine and Public Health, University of Newcastle, Newcastle, Australia
Hunter Medical Research Institute, Newcastle, New South Wales, Australia
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differentiated thyroid cancer (DTC), TSHR is therapeutically targeted to maximize radioiodine uptake into malignant thyrocytes by transiently upregulating the sodium–iodide symporter (NIS) through TSH stimulation, either endogenously through thyroid hormone
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glioblastoma ( Killela et al . 2013 , Liu et al . 2013 a ) as well as thyroid cancer ( Liu et al . 2013 b ). There are two common recurrent TERT promoter mutations in human cancer that are located at two hotspots: chr5, 1,295,228 C>T (C228T) and 1
Endocrinology Service of Institute Orizonti, Belo Horizonte, Minas Gerais, Brazil
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Biotechnology Post-graduation Program, Federal University of São Paulo, São Paulo, Brazil
Estructural and Functional Biology Program, Federal University of São Paulo, São Paulo, Brazil
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Biotechnology Post-graduation Program, Federal University of São Paulo, São Paulo, Brazil
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Post-Graduation Program Molecular Medicine, Faculty of Medicine, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Endocrinology Service of Hospital das Clínicas, Federal University of Minas Gerais, Belo Horizonte, Brazil
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Post-Graduation Program Medicine and Health, Faculty of Medical Sciences, Federal University of Bahia, Salvador, Bahia, Brazil
Post-Graduate Program in Interactive Processes of Organs and Systems, Health & Science Institute, Federal University of Bahia, Salvador, Bahia, Brazil
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during life, leading to the early discovery of incidental PTCs. The possibility of a causal association instead of a direct cause-effect link in cases of co-occurrence of congenital hypothyroidism and thyroid cancer should also be considered
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Introduction Since the '40s, the treatment of distant metastases from differentiated thyroid cancer is based on the administration of a high activity of 131 I and this was the first available targeted therapy for metastatic disease that
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Introduction Among endocrine tumors, thyroid cancer is the most common, with an estimated incidence of 12.2/100 000 per year in the USA ( Howlader et al . 2013 ). The incidence of thyroid cancer, both in the USA and worldwide, has been increasing
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). In cell lines derived from follicular and papillary thyroid cancers, metformin inhibited cell growth, activated AMPK, down-regulated p70S6K/pS6 signaling, antagonized the growth-stimulatory effects of insulin, inhibited clonal cell growth, and reduced