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Maria Denaro Department of Surgical Pathology Medical, Molecular and Critical Area, University of Pisa, Pisa, Italy

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Clara Ugolini Department of Laboratory Medicine Section of Pathology Azienda Ospedaliero-Universitaria Pisana, Pisa, Italy

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Anello Marcello Poma Department of Surgical Pathology Medical, Molecular and Critical Area, University of Pisa, Pisa, Italy

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Nicla Borrelli Department of Surgical Pathology Medical, Molecular and Critical Area, University of Pisa, Pisa, Italy

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Gabriele Materazzi Department of Surgical Pathology Medical, Molecular and Critical Area, University of Pisa, Pisa, Italy

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Paolo Piaggi National Institute of Diabetes and Digestive and Kidney Diseases Phoenix, Arizona, USA

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Massimo Chiarugi Department of Surgical Pathology Medical, Molecular and Critical Area, University of Pisa, Pisa, Italy

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Paolo Miccoli Department of Surgical Pathology Medical, Molecular and Critical Area, University of Pisa, Pisa, Italy

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Paolo Vitti Department of Clinical and Experimental Medicine University of Pisa, Pisa, Italy

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Fulvio Basolo Department of Surgical Pathology Medical, Molecular and Critical Area, University of Pisa, Pisa, Italy

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-pathological features such as age, sex, tumor size and aggressive behavior ( Yip et al. 2011 , Wang et al. 2013 ). Some studies have evaluated the association between genetic alterations and miRNA expression in papillary thyroid carcinomas (PTCs), but the results

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E Fiore Department of Endocrinology, Department of Electrical Systems and Automation, Section of Pathology, Section of Cytopathology, Department of Surgery, University of Pisa, via Paradisa 2, 56100 Pisa, Italy

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T Rago Department of Endocrinology, Department of Electrical Systems and Automation, Section of Pathology, Section of Cytopathology, Department of Surgery, University of Pisa, via Paradisa 2, 56100 Pisa, Italy

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F Latrofa Department of Endocrinology, Department of Electrical Systems and Automation, Section of Pathology, Section of Cytopathology, Department of Surgery, University of Pisa, via Paradisa 2, 56100 Pisa, Italy

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M A Provenzale Department of Endocrinology, Department of Electrical Systems and Automation, Section of Pathology, Section of Cytopathology, Department of Surgery, University of Pisa, via Paradisa 2, 56100 Pisa, Italy

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P Piaggi Department of Endocrinology, Department of Electrical Systems and Automation, Section of Pathology, Section of Cytopathology, Department of Surgery, University of Pisa, via Paradisa 2, 56100 Pisa, Italy

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A Delitala Department of Endocrinology, Department of Electrical Systems and Automation, Section of Pathology, Section of Cytopathology, Department of Surgery, University of Pisa, via Paradisa 2, 56100 Pisa, Italy

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M Scutari Department of Endocrinology, Department of Electrical Systems and Automation, Section of Pathology, Section of Cytopathology, Department of Surgery, University of Pisa, via Paradisa 2, 56100 Pisa, Italy

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F Basolo Department of Endocrinology, Department of Electrical Systems and Automation, Section of Pathology, Section of Cytopathology, Department of Surgery, University of Pisa, via Paradisa 2, 56100 Pisa, Italy

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G Di Coscio Department of Endocrinology, Department of Electrical Systems and Automation, Section of Pathology, Section of Cytopathology, Department of Surgery, University of Pisa, via Paradisa 2, 56100 Pisa, Italy

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L Grasso Department of Endocrinology, Department of Electrical Systems and Automation, Section of Pathology, Section of Cytopathology, Department of Surgery, University of Pisa, via Paradisa 2, 56100 Pisa, Italy

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A Pinchera Department of Endocrinology, Department of Electrical Systems and Automation, Section of Pathology, Section of Cytopathology, Department of Surgery, University of Pisa, via Paradisa 2, 56100 Pisa, Italy

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P Vitti Department of Endocrinology, Department of Electrical Systems and Automation, Section of Pathology, Section of Cytopathology, Department of Surgery, University of Pisa, via Paradisa 2, 56100 Pisa, Italy

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probability that mutated oncogenes may cause cancer clinically detectable. PTC frequently has genetic alterations leading to the activation of the mitogen-activated protein kinase signaling pathway. Most common mutations in PTC are point mutations of the BRAF

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Toyoshi Endo Third Department of Internal Medicine, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo City, Yamanashi 409-3898, Japan

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Tetsuro Kobayashi Third Department of Internal Medicine, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo City, Yamanashi 409-3898, Japan

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-stimulating hormone (TSH; Nikiforov & Nikiforova 2011 ). The RET/PTC rearrangement and the BRAF V600E point mutation are the two most common genetic alterations associated with PTCs; the prevalence of RET/PTC varies from 2.5 to 78% ( Zou et al . 1994

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Esther Korpershoek Departments of Pathology, Neurology, Department of Paediatric Oncology and Haematology, Josephine Nefkens Institute, Erasmus Medical Centre, University Medical Centre Rotterdam, PO Box 2040, 3000 CA Rotterdam, The Netherlands

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Nanne K Kloosterhof Departments of Pathology, Neurology, Department of Paediatric Oncology and Haematology, Josephine Nefkens Institute, Erasmus Medical Centre, University Medical Centre Rotterdam, PO Box 2040, 3000 CA Rotterdam, The Netherlands
Departments of Pathology, Neurology, Department of Paediatric Oncology and Haematology, Josephine Nefkens Institute, Erasmus Medical Centre, University Medical Centre Rotterdam, PO Box 2040, 3000 CA Rotterdam, The Netherlands

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Angelique Ziel-van der Made Departments of Pathology, Neurology, Department of Paediatric Oncology and Haematology, Josephine Nefkens Institute, Erasmus Medical Centre, University Medical Centre Rotterdam, PO Box 2040, 3000 CA Rotterdam, The Netherlands

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Hanneke Korsten Departments of Pathology, Neurology, Department of Paediatric Oncology and Haematology, Josephine Nefkens Institute, Erasmus Medical Centre, University Medical Centre Rotterdam, PO Box 2040, 3000 CA Rotterdam, The Netherlands

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Lindsey Oudijk Departments of Pathology, Neurology, Department of Paediatric Oncology and Haematology, Josephine Nefkens Institute, Erasmus Medical Centre, University Medical Centre Rotterdam, PO Box 2040, 3000 CA Rotterdam, The Netherlands

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Jan Trapman Departments of Pathology, Neurology, Department of Paediatric Oncology and Haematology, Josephine Nefkens Institute, Erasmus Medical Centre, University Medical Centre Rotterdam, PO Box 2040, 3000 CA Rotterdam, The Netherlands

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Winand N M Dinjens Departments of Pathology, Neurology, Department of Paediatric Oncology and Haematology, Josephine Nefkens Institute, Erasmus Medical Centre, University Medical Centre Rotterdam, PO Box 2040, 3000 CA Rotterdam, The Netherlands

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Ronald R de Krijger Departments of Pathology, Neurology, Department of Paediatric Oncology and Haematology, Josephine Nefkens Institute, Erasmus Medical Centre, University Medical Centre Rotterdam, PO Box 2040, 3000 CA Rotterdam, The Netherlands

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appeared to be no difference in frequencies between benign or malignant tumours ( Petri et al . 2008 ). Genetic alterations have been investigated by CGH in two Pten KO mouse models ( You et al . 2002 , Korpershoek et al . 2009 ). The first study

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Wenzel M Hackeng Department of Pathology, University Medical Center Utrecht, Utrecht, The Netherlands

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Lodewijk A A Brosens Department of Pathology, University Medical Center Utrecht, Utrecht, The Netherlands

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Koen M A Dreijerink Department of Pathology, University Medical Center Utrecht, Utrecht, The Netherlands
Department of Endocrinology, Amsterdam University Medical Centers, VU University Medical Center, Amsterdam, The Netherlands

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vs aggressive insulinomas The low incidence of aggressive insulinomas has resulted in few data on genetic alterations in these tumors. The first evidence of biological differences between indolent and aggressive insulinomas was discovered by

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Devora Champa
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Marika A Russo
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Xiao-Hui Liao Department of Developmental and Molecular Biology, Departments of Medicine, Pediatrics and Committee on Genetics, Department of Pathology, Albert Einstein College of Medicine, Price Center for Genetic and Translational Medicine, 1301 Morris Park Avenue, Room 302, Bronx, New York 10461, USA

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Samuel Refetoff Department of Developmental and Molecular Biology, Departments of Medicine, Pediatrics and Committee on Genetics, Department of Pathology, Albert Einstein College of Medicine, Price Center for Genetic and Translational Medicine, 1301 Morris Park Avenue, Room 302, Bronx, New York 10461, USA
Department of Developmental and Molecular Biology, Departments of Medicine, Pediatrics and Committee on Genetics, Department of Pathology, Albert Einstein College of Medicine, Price Center for Genetic and Translational Medicine, 1301 Morris Park Avenue, Room 302, Bronx, New York 10461, USA

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Ronald A Ghossein Department of Developmental and Molecular Biology, Departments of Medicine, Pediatrics and Committee on Genetics, Department of Pathology, Albert Einstein College of Medicine, Price Center for Genetic and Translational Medicine, 1301 Morris Park Avenue, Room 302, Bronx, New York 10461, USA

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Antonio Di Cristofano
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of whether these tumors are sensitive to the inhibition of MEK1 and MEK2. We used two cell lines derived from our mouse model, as well as a human ATC cell line, Cal62, which harbors the same genetic alterations and thus represents an appropriate human

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Elizabeth J de Koster Department of Medical Imaging, Nuclear Medicine, Radboud University Medical Centre, Nijmegen, the Netherlands
Department of Radiology, Section of Nuclear Medicine, Leiden University Medical Center, Leiden, the Netherlands

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

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Lioe-Fee de Geus-Oei Department of Medical Imaging, Nuclear Medicine, Radboud University Medical Centre, Nijmegen, the Netherlands
Department of Radiology, Section of Nuclear Medicine, Leiden University Medical Center, Leiden, the Netherlands
Biomedical Photonic Imaging Group, University of Twente, Enschede, the Netherlands

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Wim J G Oyen Department of Medical Imaging, Nuclear Medicine, Radboud University Medical Centre, Nijmegen, the Netherlands
Department of Radiology and Nuclear Medicine, Rijnstate Hospital, Arnhem, the Netherlands
Department of Biomedical Sciences and Humanitas Clinical and Research Centre, Department of Nuclear Medicine, Humanitas University, Milan, Italy

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Dina Ruano Department of Pathology, Leiden University Medical Center, Leiden, the Netherlands

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Abbey Schepers Department of Surgery, Leiden University Medical Center, Leiden, the Netherlands

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Marieke Snel Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, the Netherlands

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Tom van Wezel Department of Pathology, Leiden University Medical Center, Leiden, the Netherlands

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Dennis Vriens Department of Radiology, Section of Nuclear Medicine, 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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clearly distinguished from true OCN, as it is different in both origin and genetic alterations. It may occur in lymphocytic thyroiditis, oncocytic variant papillary thyroid carcinoma, medullary thyroid carcinoma, parathyroid lesions, and non

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Marianne E Pavel Medical Department, Division of Hepatology and Gastroenterology including Metabolic Diseases, Campus Virchow Klinikum, Charité Universitätsmedizin Berlin, Berlin, Germany

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network behavior in the context of specific genetic alterations can have an influence on therapy. Since 2005, I am involved in the activities of the ENETS, where I participate in consensus meetings for the construction of guidelines for diagnosis and

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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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B Kwabi-Addo Department of Pathology, Baylor College of Medicine and Michael E DeBakey Department of Veterans Affairs Medical Center, Houston, Texas 77030, USA

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M Ozen Department of Pathology, Baylor College of Medicine and Michael E DeBakey Department of Veterans Affairs Medical Center, Houston, Texas 77030, USA

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M Ittmann Department of Pathology, Baylor College of Medicine and Michael E DeBakey Department of Veterans Affairs Medical Center, Houston, Texas 77030, USA

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other genetic alterations. A major goal is to understand the underlying differences in signal transduction between FGFR-1 and FGFR-2 that could lead to enhancement or inhibition of tumor progression by these two related receptors. In this regard

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