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William R Doerfler Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, Pennysylvania, USA

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Alyaksandr V Nikitski Department of Pathology, University of Pittsburgh, Pittsburgh, Pennysylvania, USA

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Elena M Morariu Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, Pennysylvania, USA

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N Paul Ohori Department of Pathology, University of Pittsburgh, Pittsburgh, Pennysylvania, USA

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Simion I Chiosea Department of Pathology, University of Pittsburgh, Pittsburgh, Pennysylvania, USA

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Michael S Landau Department of Pathology, University of Pittsburgh, Pittsburgh, Pennysylvania, USA

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Marina N Nikiforova Department of Pathology, University of Pittsburgh, Pittsburgh, Pennysylvania, USA

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Yuri E Nikiforov Department of Pathology, University of Pittsburgh, Pittsburgh, Pennysylvania, USA

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Linwah Yip Division of Endocrine Surgery, University of Pittsburgh, Pittsburgh, Pennysylvania, USA

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Pooja Manroa Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, Pennysylvania, USA
Division of Endocrinology, University of Texas Medical Branch, Galveston, Texas, USA

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reported widespread DNA copy number alterations (CNA), typically leading to near complete genome haploidization, as a likely genetic mechanism of HCC ( Corver et al. 2012 ). This type of CNA involved multiple chromosomes with chromosome-wide monosomy and

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Andreas Venizelos K.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Oncology, Haukeland University Hospital, Bergen, Norway

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Hege Elvebakken Department of Oncology, Ålesund Hospital, Møre og Romsdal Hospital Trust, Ålesund, Norway
Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway

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Aurel Perren Institute of Pathology, University of Bern, Bern, Switzerland

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Oleksii Nikolaienko K.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Oncology, Haukeland University Hospital, Bergen, Norway

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Wei Deng K.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Oncology, Haukeland University Hospital, Bergen, Norway

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Inger Marie B Lothe Department of Pathology, Oslo University Hospital, Oslo, Norway

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Anne Couvelard Department of Pathology, Université de Paris, Bichat Hospital, AP-HP, Paris, France

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Geir Olav Hjortland Department of Oncology, Oslo University Hospital, Oslo, Norway

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Anna Sundlöv Departmentt of Oncology, Skåne University Hospital, Lund, Sweden
Department of Medical Radiation Physics, Lund University, Lund, Sweden

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Johanna Svensson Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden

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Harrish Garresori Department of Oncology, Stavanger University Hospital, Stavanger, Norway

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Christian Kersten Department of Research, Hospital of Southern Norway, Kristiansand, Norway

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Eva Hofsli Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway
Department of Oncology, St.Olavs Hospital, Trondheim, Norway

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Sönke Detlefsen Department of Pathology, Odense University Hospital, Odense, Denmark
Department of Clinical Medicine, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark

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Merete Krogh Department of Oncology, Odense University Hospital, Odense, Denmark

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Halfdan Sorbye Department of Oncology, Haukeland University Hospital, Bergen, Norway
Department of Clinical Science, University of Bergen, Bergen, Norway

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Stian Knappskog K.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Oncology, Haukeland University Hospital, Bergen, Norway

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molecular mechanisms and genetic origin of these tumours as well as why these cancers are so aggressive. Importantly, we reveal a high fraction of targetable alterations in HG GEP-NEN patients, pointing to novel treatment strategies applying tailored

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J T W Kwon Department of Oncology, University of Oxford, Oxford, UK

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R J Bryant Department of Oncology, University of Oxford, Oxford, UK
Nuffield Department of Surgical Sciences, University of Oxford, Oxford, UK

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E E Parkes Department of Oncology, University of Oxford, Oxford, UK

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). Furthermore, advanced-stage disease in most cases develops resistance to ADT, underscoring the unmet clinical need to develop new treatments for metastatic castration-resistant PCa (mCRPC). Although the effects of DNA repair defects and genetic

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Chi-Yu Kuo Department of Surgery, MacKay Memorial Hospital and Mackay Medical College, Taipei, Taiwan

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Yuan-Ching Chang Department of Surgery, MacKay Memorial Hospital and Mackay Medical College, Taipei, Taiwan

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Ming-Nan Chien Division of Endocrinology and Metabolism, Department of Internal Medicine, MacKay Memorial Hospital and Mackay Medical College, Taipei, Taiwan

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Jie-Yang Jhuang Department of Pathology, MacKay Memorial Hospital and Mackay Medical College, Taipei, Taiwan

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Yi-Chiung Hsu Department of Biomedical Sciences and Engineering, National Central University, Taoyuan City, Taiwan

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Shih-Yuan Huang Department of Medical Research, MacKay Memorial Hospital, Taipei, Taiwan

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Shih-Ping Cheng Department of Surgery, MacKay Memorial Hospital and Mackay Medical College, Taipei, Taiwan
Department of Medical Research, MacKay Memorial Hospital, Taipei, Taiwan
Department of Pharmacology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan

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inhibition showed similar effects as the genetic silencing of SREBF1 in thyroid cancer cells. Figure 4 Alterations in metabolism, cell morphology, and motility following treatment with fatostatin, an inhibitor of SREBP1 activation. BHT-101 and FTC

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Livia Lamartina Gustave Roussy, Department of Nuclear Medicine and Endocrine Oncology, Villejuif, France

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Nadège Anizan Department of Medical Physics, Gustave Roussy and University Paris Saclay, Villejuif, France

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Corinne Dupuy UMR 8200/9019 CNRS Paris-Saclay, Genome Integrity and Cancers, Gustave Roussy and University Paris Saclay, Villejuif, France

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Sophie Leboulleux Gustave Roussy, Department of Nuclear Medicine and Endocrine Oncology, Villejuif, France

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Martin Schlumberger Gustave Roussy, Department of Nuclear Medicine and Endocrine Oncology, Villejuif, France

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intense TSH stimulation should be performed before any administration of 131 I in thyroid cancer patients. Furthermore, several alterations in the post-translational modification and targeting of NIS protein to the plasma membrane and in its degradation

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Justine Vanhevel Clinical and Experimental Endocrinology, Department of Chronic Diseases and Metabolism (CHROMETA), KU Leuven, Leuven, Belgium

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Lieve Verlinden Clinical and Experimental Endocrinology, Department of Chronic Diseases and Metabolism (CHROMETA), KU Leuven, Leuven, Belgium

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Stefanie Doms Clinical and Experimental Endocrinology, Department of Chronic Diseases and Metabolism (CHROMETA), KU Leuven, Leuven, Belgium

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Hans Wildiers UZ Leuven, General Medical Oncology and Multidisciplinary Breast Center, Leuven, Belgium

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Annemieke Verstuyf Clinical and Experimental Endocrinology, Department of Chronic Diseases and Metabolism (CHROMETA), KU Leuven, Leuven, Belgium

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precursor, 7-dehydrocholesterol ( Leyssens et al. 2013 , Christakos et al. 2016 , 2019 , Jeon & Shin 2018 ). Since exposure to sunlight is a major trigger for vitamin D 3 synthesis in the skin, alterations in sunlight exposure based on season and

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James F H Pittaway Centre for Endocrinology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK

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Constantinos Lipsos Centre for Endocrinology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK

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Katia Mariniello Centre for Endocrinology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK

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Leonardo Guasti Centre for Endocrinology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK

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and mRNA level ( Luo et al. 2006 , Dezső et al. 2008 ). Recently, a large pangenomic analysis of hepatoblastoma has revealed that upregulation of imprinted genes from the 14q32 locus, including DLK1 , is a genetic hallmark of the malignancy

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