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Huy Gia Vuong, Nguyen Phuoc Long, Nguyen Hoang Anh, Tran Diem Nghi, Mai Van Hieu, Le Phi Hung, Tadao Nakazawa, Ryohei Katoh and Tetsuo Kondo

.68–3.37; I 2  = 0%). Figure 3 Forest plots examined the clinicopathological significance between PTC-TCF and classical PTC in multifocality (A), extrathyroidal extension (B), lymph node metastasis (C), pT3 – T4 (D), distant metastasis (E) and BRAF

Open access

Huy Gia Vuong, Uyen N P Duong, Ahmed M A Altibi, Hanh T T Ngo, Thong Quang Pham, Hung Minh Tran, Greta Gandolfi and Lewis Hassell

pathogenesis in PTC. Several genetic alterations have been described in PTC ( 4 ). Among them, BRAF mutation, especially BRAF V600E , is the most common mutation in PTC; however, its prognostic role in PTC is still debated ( 5 , 6 , 7 ). Another recently

Open access

Lauren E Henke, John D Pfeifer, Thomas J Baranski, Todd DeWees and Perry W Grigsby

are mutations in the BRAF gene. Occurring in approximately 50% of PTC patients, the BRAF mutation causes constitutive activation of the MAP-kinase pathway, leading to increased propensity for tumor cell proliferation ( 16 , 17 ). Although the

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Barbora Pekova, Sarka Dvorakova, Vlasta Sykorova, Gabriela Vacinova, Eliska Vaclavikova, Jitka Moravcova, Rami Katra, Petr Vlcek, Pavla Sykorova, Daniela Kodetova, Josef Vcelak and Bela Bendlova

only in clinical-pathological features, but also in genetic alterations. Main PTC-activating somatic mutations in the RAS , BRAF and TERT genes and RET/PTC rearrangements cause uncontrolled activation of MAPK and PI3K signaling pathways. It was

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Catarina Tavares, Maria João Coelho, Catarina Eloy, Miguel Melo, Adriana Gaspar da Rocha, Ana Pestana, Rui Batista, Luciana Bueno Ferreira, Elisabete Rios, Samia Selmi-Ruby, Bruno Cavadas, Luísa Pereira, Manuel Sobrinho Simões and Paula Soares

understood, but some studies demonstrated that both mRNA and protein are differentially expressed according to the genetic background of the tumor. In fact, papillary thyroid carcinomas (PTCs) harboring the BRAF V600E mutation present lower SLC5A5 mRNA and

Open access

Tiemo S Gerber, Arno Schad, Nils Hartmann, Erik Springer, Ulrich Zechner and Thomas J Musholt

of the percentage of malignant cells (tumour cell to non-tumour cell). An overview of the patient data is presented in Table 1 . Routine Sanger sequencing was performed on the BRAF V600E and BRAF wild-type V600 gene locus. Table 1

Open access

Guoquan Zhu, Yuying Deng, Liqin Pan, Wei Ouyang, Huijuan Feng, Juqing Wu, Pan Chen, Jing Wang, Yanying Chen and Jiaxin Luo

metastasis. In recent years, an increasing number of molecular genetic characteristics associated with invasiveness and clinical management have been uncovered, including the BRAF V600E mutation, TERT promoter mutations, RAS mutations and RET

Open access

Dario de Biase, Federica Torricelli, Moira Ragazzi, Benedetta Donati, Elisabetta Kuhn, Michela Visani, Giorgia Acquaviva, Annalisa Pession, Giovanni Tallini, Simonetta Piana and Alessia Ciarrocchi

-library preparation. The custom panel included the following targeted gene regions: BRAF (exon 15), KRAS (exons 2, 3, 4), NRAS (exons 2, 3, 4), HRAS (exons 2, 3), EGFR (exons 12, 18, 19, 20, 21), CTNNB1 (exon 3), EIF1AX (exons 1, 2), GNAS (exons 8, 9

Open access

June Young Choi, Jin Wook Yi, Jun Hyup Lee, Ra-Yeong Song, Hyeongwon Yu, Hyungju Kwon, Young Jun Chai, Su-jin Kim and Kyu Eun Lee

Center. Mutation status of BRAF , RAS ( NRAS , HRAS and KRAS ) and VDR genes was identified from somatic mutation calling files: identical results in two different calling files were considered as a meaningful mutation. TCGA gene expression data

Open access

Ashley N Reeb, Andrea Ziegler and Reigh-Yi Lin

. The mutational characteristics of these human FTC cell lines, based on published reports ( 7 , 8 , 15 ), are summarized below. FTC-238 and TT2609-CO2 each has a TP53 mutation, and WRO has a BRAF V600E mutation. None of the cell lines have