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Weill-Cornell Medical College, New York, New York, USA
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Weill-Cornell Medical College, New York, New York, USA
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Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA
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Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
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Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
Weill-Cornell Medical College, New York, New York, USA
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most prevalent form of the disease, are associated with clonal non-overlapping activating mutations of genes encoding MAPK pathway signaling effectors, primarily point mutations of BRAF and of the three RAS genes, as well as fusions of receptor
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Division of Endocrinology, Department of Molecular Virology, Center for Biostatistics, Diabetes and Metabolism, Department of Internal Medicine
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Division of Endocrinology, Department of Molecular Virology, Center for Biostatistics, Diabetes and Metabolism, Department of Internal Medicine
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, invasion, and metastases is important in order to develop effective targeted therapies. PTC tumorigenesis is driven largely by activation of the MAP kinase pathway through several genetic events, the most common of which are activating mutations in BRAF
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times their widths.’), and the percentage of tall cells (TCs) needed in a given tumor is defined variably in the literature ( Ostrowski & Merino 1996 , DeLellis et al . 2004 ). The oncogenic BRAF V600E mutation occurs in about 40–45% of PTCs
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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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AKT pathways occur frequently in thyroid cancers. The most common form of thyroid cancer, well-differentiated papillary thyroid cancer (PTC), is driven primarily by mutually exclusive mutations that activate MAPK signaling; ~60% have BRAF V600E
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Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Korea
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Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Korea
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sarcoma viral oncogene homolog B ( BRAF ) T1799A mutation has drawn much attention based on its high prevalence, occurring in about 45% of PTC and 25% of ATC cases and its association with PTC recurrence ( Kim et al. 2012 , Xing et al. 2015 ). However
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the most common and occurring mainly in PTC and some benign adenomas. The PAX8-PPAR γ occurs both in FTC and benign thyroid adenoma ( Cheung et al. 2003 , Sahin et al. 2005 ). The recently discovered activating mutation in BRAF (the gene for
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Department of Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia
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/PTC rearrangements, mutations in BRAF , NRAS , etc., and the PI3K/AKT pathway is activated mostly in poorly differentiated (PDTC) and anaplastic thyroid cancer (ATC) as a result of mutations in ALK , RAS , PIK3CA , AKT , etc. ( Murugan & Xing 2011 , Xing 2013
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. 2005 , Kurata et al. 2016 , Subbiah et al. 2018 , Kim et al. 2020 , Lee & Park 2021 ). The BRAF V600E mutation is one of the common genetic alterations in ATC, accounting for 20–50% of cases ( Xing 2013 , Jeon et al. 2016 , Subbiah et al
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Introduction With a rapidly increasing incidence worldwide, papillary thyroid carcinoma (PTC) represents the majority of thyroid cancer cases ( Ahn & Park 2009 , Siegel et al . 2014 ). The recently discovered BRAF V600E mutation (hereafter