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Tanner Freeman Department of Pathology, UPMC, Pittsburgh, Pennsylvania, USA

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Charit Taneja Division of Endocrinology and Metabolism, UPMC, Pittsburgh, Pennsylvania, USA

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

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Abigail I Wald Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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John Skaugen Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Linwah Yip Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Seungwon Kim Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Robert L Ferris Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
UPMC Hillman Cancer Center, Department of Oncology, Pittsburgh, Pennsylvania, USA

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

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Somak Roy Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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

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molecularly identified thyroidal metastasis of renal cell carcinoma and genetic alterations detected in FNAs by ThyroSeq testing. Case Age (y); gender Nodule size (cm) BCC Cytologic features a Multiple nodules USG History of RCC

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Jamie L Van Etten Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA

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Scott M Dehm Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA
Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA
Department of Urology, University of Minnesota, Minneapolis, MN, USA

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Nowell in 1976 based on cytogenetic data ( Nowell 1976 ). In this early model, a cell of origin acquires genetic alterations that promote neoplasia. Further genetic instability fuels clonal expansion of “fit” clones that ultimately leads to advanced

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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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William D Foulkes Departments of Human Genetics, Medicine and Oncology, McGill University, Montreal, Québec, Canada

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Jérôme Bertherat Department of Endocrinology, Cochin Hospital, Paris Descartes University, Paris, France

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Charis Eng Genomic Medicine Institute, Lerner Research Institute and Taussig Cancer Institute, Cleveland Clinic, Cleveland, Ohio, USA
Department of Genetics and Genome Sciences and Germline High Risk Focus Group, Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA

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their US and Canadian collaborators ( Goudie et al. 2018 ) this complex and evolving field is efficiently summarized. It clearly shows that almost all endocrine glands have been found to possess genetic alterations in at least one tumor susceptibility

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Adrian F Daly Department of Endocrinology Centre Hospitalier Universitaire de Liège, University of Liège, Domaine Universitaire du Sart‐Tilman, 4000 Liège, Belgium

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Albert Beckers Department of Endocrinology Centre Hospitalier Universitaire de Liège, University of Liège, Domaine Universitaire du Sart‐Tilman, 4000 Liège, Belgium

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be a pentad ( Carney 2009 ). Carney triad has long been a puzzling entity, having all of the features of a genetic disease, including multiple rare tumor types occurring metachronously or synchronously in different organs and having particularly

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Willem E Corver Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands

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Hans Morreau Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands

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Alterations as Genetic Drivers in Hürthle Cell Carcinoma’ Ganly et al . (2018) and Gopal et al . (2018) , respectively, defined alterations in oncogenic drivers and mitochondrial DNA mutations complex I (mtDNA), including the widespread whole

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M Montani
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A M Schmitt
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S Schmid
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T Locher
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P Saremaslani
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P U Heitz
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P Komminoth
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A Perren
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carcinoma. Journal of Molecular Medicine 81 819 –823. Khosla S , Patel VM, Hay ID, Schaid DJ, Grant CS, van Heerden JA & Thibodeau SN 1991 Loss of heterozygosity suggests multiple genetic alterations in pheochromocytomas

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Ashley K Clift Department of Surgery and Cancer, Imperial College London, London, UK
NHS Nightingale Hospital London, London, UK

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Andrea Frilling Department of Surgery and Cancer, Imperial College London, London, UK

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-specific alterations in genetic landscape, protein expression, pathway activity or cell biology. Theoretically, it aims to minimise the ‘off-target’ adverse effects of pharmacological agents and maximise disease response by tailoring the strategy to the personal

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Pamela Brock Divison of Human Genetics, Department of Internal Medicine and the Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, USA

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Jennifer L Geurts Department of Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin, USA

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Paulien Van Galen Hereditary Cancer Clinic and Hereditary Endocrine Clinic, Alberta Children’s Hospital, Calgary, Alberta, USA

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Erica Blouch Center for Cancer Risk Assessment, Massachusetts General Hospital, Boston, Massachusetts, USA

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James Welch Metabolic Disease Branch, National Institute of Diabetes and Digestive and Kidney Disease, National Institutes of Health, Bethesda, Maryland, USA

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Amy Kunz Allegheny Health Network Cancer Institute, Pittsburgh, Pennsylvania, USA

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Lauren Desrosiers Texas Children’s Hospital, Baylor College of Medicine, Houston, Texas, USA

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Jennifer Gauerke Center for Individualized Medicine, College of Medicine, Mayo Clinic, Rochester, Minnesota, USA

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Samuel Hyde Clinical Cancer Genetics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Introduction The goals of achieving a genetic diagnosis in the setting of hereditary endocrine neoplasia (HEN) syndromes include: to understand the basis for disease, provide anticipatory guidance for early detection (or prevention) of

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Felix Haglund Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden

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Carl Christofer Juhlin Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden
Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden
Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden

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Taylor Brown Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden
Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden

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Mehran Ghaderi Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden

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Tiantian Liu Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden

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Adam Stenman Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden

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Andrii Dinets Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden

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Manju Prasad Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden

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Reju Korah Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden
Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden

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Dawei Xu Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden

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Tobias Carling Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden
Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden

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Catharina Larsson Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK), Karolinska University Hospital, SE-171 76, Stockholm, Sweden

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telomerase activation is therefore expected to be caused by other mechanisms, which could include copy number alterations, DNA methylation, or other genetic and regulatory events. Declaration of interest The authors declare that there is no conflict of

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