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Trisha Dwight, Aidan Flynn, Kaushalya Amarasinghe, Diana E Benn, Richard Lupat, Jason Li, Daniel L Cameron, Annette Hogg, Shiva Balachander, Ida L M Candiloro, Stephen Q Wong, Bruce G Robinson, Anthony T Papenfuss, Anthony J Gill, Alexander Dobrovic, Rodney J Hicks, Roderick J Clifton-Bligh and Richard W Tothill

)), suggestive of another mechanism of TERT activation. Recently, activation of TERT as a result of structural rearrangements, leading to the placement of enhancers proximal to the TERT promoter have been described in a number of cancer types ( Davis et al

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Gahee Park, Tae Hyuk Kim, Hae-Ock Lee, Jung Ah Lim, Jae-Kyung Won, Hye Sook Min, Kyu Eun Lee, Do Joon Park, Young Joo Park and Woong-Yang Park

://www.nccn.org/professionals/physician_gls/pdf/thyroid.pdf ; accessed 26th April 2014). Identification of the mutations driving DTC prompted the therapeutic use of oral multikinase inhibitors such as sorafenib, which targets rearranged during transfection (RET), v-raf murine sarcoma viral oncogene homolog B (BRAF

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Kristian Unger, Johannes Wienberg, Andrew Riches, Ludwig Hieber, Axel Walch, Andreas Brown, Patricia C M O'Brien, Cäcilia Briscoe, Lindsey Gray, Elke Rodriguez, Gerhard Jackl, Jeroen Knijnenburg, Giovanni Tallini, Malcolm Ferguson-Smith and Horst Zitzelsberger

Introduction Chromosome rearrangement is a key mechanism for gene alteration and subsequent deregulation of cellular processes such as proliferation, apoptosis, genome stability, angiogenesis and motility, leading to malignant tumour

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Raffaele Ciampi, Thomas J Giordano, Kathryn Wikenheiser-Brokamp, Ronald J Koenig and Yuri E Nikiforov

(reviewed in Ciampi & Nikiforov 2005 , Xing 2005 ). Recently, BRAF has also been shown to be activated in papillary carcinomas by chromosomal rearrangement resulting in the AKAP9-BRAF fusion ( Ciampi et al. 2005 ). It is a rare event in sporadic

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Viktoria Evdokimova, Manoj Gandhi, Jayanagendra Rayapureddi, James R Stringer and Yuri E Nikiforov

higher doses ( Ron et al . 1995 , Cardis et al . 2005 a , b ). Over the last decade, strong evidence has been accumulated supporting the central role of chromosomal rearrangements in carcinogenesis initiated by IR ( Ciampi et al . 2005 , Gandhi et

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Stéphanie Durand, Carole Ferraro-Peyret, Mireille Joufre, Annie Chave, Françoise Borson-Chazot, Samia Selmi-Ruby and Bernard Rousset

Introduction Papillary thyroid carcinomas (PTC), the most common forms of thyroid cancer, are characterized by two main gene alterations, either a rearrangement of RET gene or a point mutation of BRAF gene. As the result of a somatic chromosomal

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Cristina Romei, Raffaele Ciampi, Pinuccia Faviana, Laura Agate, Eleonora Molinaro, Valeria Bottici, Fulvio Basolo, Paolo Miccoli, Furio Pacini, Aldo Pinchera and Rossella Elisei

not responsive to conventional 131-Iodine radiotherapy ( Haugen 1999 ). RET gene rearrangements, BRAF and RAS oncogene point mutations, which can activate the mitogen-activated protein (MAP) kinase signaling pathway, have been highly studied in PTC and

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J Lado-Abeal, R Celestino, S B Bravo, M E R Garcia-Rendueles, J de la Calzada, I Castro, P Castro, C Espadinha, F Palos, P Soares, C V Alvarez, M Sobrinho-Simões and J Cameselle-Teijeiro

proliferator-activated receptor gamma ( PPAR γ ) rearrangement ( Kroll et al . 2005 ) is highly prevalent in follicular thyroid carcinoma (FTC), correlating with an angioinvasive phenotype ( Marques et al . 2002 , Nikiforova et al . 2002 ). PAX8 – PPAR γ

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J Di Cristofaro, V Vasko, V Savchenko, S Cherenko, A Larin, M D Ringel, M Saji, M Marcy, J F Henry, P Carayon and C De Micco

found among liquidators exposed during recovery work from April to July 1986, when the risk of internal irradiation of the thyroid with incorporated 131 I was greatest. Occurrence of ret oncogene rearrangements involving several different

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Giovanna Maria Pierantoni, Palma Finelli, Emanuele Valtorta, Daniela Giardino, Ornella Rodeschini, Francesco Esposito, Marco Losa, Alfredo Fusco and Lidia Larizza

et al. 1994 ). HMGA proteins play a crucial role in the process of cancerogenesis. In fact, chromosomal translocations of 12q13-15, involving the HMGA2 gene, leading to rearrangements and dysregulated expression of the HMGA2 gene, have been