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Luca Morandi, Alberto Righi, Francesca Maletta, Paola Rucci, Fabio Pagni, Marco Gallo, Sabrina Rossi, Leonardo Caporali, Anna Sapino, Ricardo V Lloyd, and Sofia Asioli

because the HPTC cells seem to be scarcely responsive to 131I treatment ( Haugen et al . 2016 ). To date, in PTC, the common known mutations are represented by several RET/PTC rearrangements ( Romei & Elisei 2012 ), BRAF p.V600 mutation ( Mathur et

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Thomas G Papathomas, Lindsey Oudijk, Ellen C Zwarthoff, Edward Post, Floor A Duijkers, Max M van Noesel, Leo J Hofland, Patrick J Pollard, Eamonn R Maher, David F Restuccia, Richard A Feelders, Gaston J H Franssen, Henri J Timmers, Stefan Sleijfer, Wouter W de Herder, Ronald R de Krijger, Winand N M Dinjens, and Esther Korpershoek

demonstrated that activation of telomerase via transcriptional TERT upregulation can be caused by mutations in the core promoter region of TERT (Chr5) with 1 295 28 C>T, 1 295 250 C>T being the two most frequent mutation hotspots ( Horn et al . 2013 , Huang

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Louis de Mestier, Jean-Baptiste Danset, Cindy Neuzillet, Vinciane Rebours, Jérôme Cros, Nadem Soufir, and Pascal Hammel

lesions and personalized therapy. Germline mutations have been described in BRCA2 , BRCA1 , p16/CDKN2A , PALB2 , PRSS1 , STK11 , TP53 , ATM and Lynch syndrome-associated genes ( Klein 2012 , Salo-Mullen et al. 2015 , Zhen et al. 2015 , Hu

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Vassiliki Kotoula, Elias Sozopoulos, Helen Litsiou, Galinos Fanourakis, Triantafyllia Koletsa, Gerassimos Voutsinas, Sophia Tseleni-Balafouta, Constantine S Mitsiades, Axel Wellmann, and Nicholas Mitsiades

the epidermal growth factor receptor (EGFR, also known as HER1, a member of the HER family of transmembrane receptors), to the p42/p44 MAP kinases (ERK1/2), the key effectors of this pathway. Activating mutations of BRAF exons 11 and 15 occur

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Ebtesam Qasem, Avaniyapuram Kannan Murugan, Hindi Al-Hindi, Mingzhao Xing, Mai Almohanna, Meshael Alswailem, and Ali S Alzahrani

et al . 2009 ). Major progress in our understanding of the molecular pathogenesis of DTC has taken place over the last decade ( Xing 2013 ). The contribution of genetic mutations in the MAPK and phosphatidylinositide 3-kinases (PI3KCa)-AKT pathways in

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A Raitila, M Georgitsi, A Karhu, K Tuppurainen, M J Mäkinen, K Birkenkamp-Demtröder, K Salmenkivi, T F Ørntoft, J Arola, V Launonen, P Vahteristo, and L A Aaltonen

Introduction Germline mutations in the aryl hydrocarbon receptor interacting protein ( AIP ) gene were recently reported in patients with pituitary adenoma predisposition (PAP; Vierimaa et al. 2006 ). Typically, individuals with

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Yulong Li, Jianhua Zhang, Poorni R Adikaram, James Welch, Bin Guan, Lee S Weinstein, Haobin Chen, and William F Simonds

-stage diagnosis and increased chance of cure. CDC73 , formerly known as HRPT2 , is a key gene implicated in development of parathyroid cancer. It is a putative tumor suppressor gene with 17 exons ( Fig. 1 ), and multiple germline and somatic mutations have been

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Jenny Welander, Adam Andreasson, Michael Brauckhoff, Martin Bäckdahl, Catharina Larsson, Oliver Gimm, and Peter Söderkvist

hereditary tumor syndromes such as multiple endocrine neoplasia type 2 (MEN2), von Hippel–Lindau disease (VHL), neurofibromatosis type 1 (NF1) or familial pheochromocytoma–paraganglioma syndrome, which are caused by mutations in the genes RET , VHL , NF1

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Esther Korpershoek, Bart-Jeroen Petri, Francien H van Nederveen, Winand N M Dinjens, Albert A Verhofstad, Wouter W de Herder, Sonja Schmid, Aurel Perren, Paul Komminoth, and Ronald R de Krijger

germline mutations of the RET protooncogene, which are mostly (80–96%) found in RET exons 10, 11, and 16 ( Thakker 2001 , Peczkowska & Januszewicz 2005 ). Somatic RET mutations have also been found in sporadic PCC affecting exons 10, 11, and 16

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Rengyun Liu and Mingzhao Xing

), and galectin 3 ( Bartolazzi et al . 2008 ) and prognostically BRAF V600E mutation ( Xing et al . 2013 b , 2014 a ). However, the diagnostic and prognostic accuracies of these markers still have much room for improvement and new markers are