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Paola Caria, Tinuccia Dettori, Daniela V Frau, Angela Borghero, Antonello Cappai, Alessia Riola, Maria L Lai, Francesco Boi, Piergiorgio Calò, Angelo Nicolosi, Stefano Mariotti and Roberta Vanni

knowledge regarding the molecular pathways implicated in papillary thyroid carcinoma (PTC) pathobiology has revealed that BRAF V600E mutation, rearrangements of the tyrosine kinase receptor genes RET and TRK ( NTRK1 ), and RAS mutations play material

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Lois M Mulligan

improve outcomes. The rearranged during transfection (RET) proto-oncogene represents a paradigm for the power of molecular medicine to drive changes in diagnosis and patient management that alter disease outcomes and patient quality of life. Originally

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Sara Redaelli, Ivan Plaza-Menacho and Luca Mologni

et al. 1997 ). At that time, it was known to be frequently rearranged in papillary thyroid cancers (PTC), but its involvement in MEN2 and MTC was not yet clear ( Grieco et al. 1990 , Santoro et al. 1990 ). The paper by Mulligan and colleagues

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Vincenzo Marotta, Concetta Sciammarella, Annamaria Colao and Antongiulio Faggiano

to DTC, including BRAF and RAS point mutations and RET/PTC rearrangements, in the prognostic setting ( Nikiforov & Nikiforova 2011 , Xing 2013 ). Afterwards, we will discuss about the recent findings and possible prognostic role of some emerging

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J Di Cristofaro, M Silvy, A Lanteaume, M Marcy, P Carayon and C De Micco

). Oncogene defects Oncogene mutations and rearrangements are summarized in Table 5 . All Nras mutations occurred at codon 61 (exon 2), with equal incidence of transition and transversion. Mutations were present in 38.1% of FC, 25% of PCfv, 10% of

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Delila Gasi Tandefelt, Joost Boormans, Karin Hermans and Jan Trapman

rearrangement between the first exon(s) of TMPRSS2 and the ERG oncogenes ( Fig. 2 ; Tomlins et al . 2005 ). This latter finding was rapidly confirmed and extended by others, and it is now generally accepted that over half of prostate cancers harbor the

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M Xing

alterations, some of which are seen only in this cancer. The classical oncogenic genetic alterations commonly seen in thyroid cancer include Ras mutations ( Fagin 2002 , Bongarzone & Pierotti 2003 ), RET/PTC rearrangements ( Nikiforov 2002 , Santoro et

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E Puxeddu, J A Knauf, M A Sartor, N Mitsutake, E P Smith, M Medvedovic, C R Tomlinson, S Moretti and J A Fagin

Introduction Rearrangements of the protooncogene RET resulting in its constitutive activation are believed to play a causative role in the pathogenesis of a significant proportion of papillary carcinomas of the thyroid (PTC

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Isabel Amendoeira, Tiago Maia and Manuel Sobrinho-Simões

, Cho et al . 2017 ). It is easy to separate the molecular profile of cPTC (‘ BRAF V600E -like genotype’) in which there are frequent RET/PTC and NTRK rearrangements and less frequent RAS mutations, from the molecular profile of E-FVPTC (‘ RAS

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Debora Degl'Innocenti, Paola Romeo, Eva Tarantino, Marialuisa Sensi, Giuliana Cassinelli, Veronica Catalano, Cinzia Lanzi, Federica Perrone, Silvana Pilotti, Ettore Seregni, Marco A Pierotti, Angela Greco and Maria Grazia Borrello

patients present with recurrences and distant metastases. Four different alternative genetic lesions have been identified as driving oncogenic alterations in ∼70% of PTCs, including RET/PTK or TRK rearrangements and BRAF or RAS mutations. All these