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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

metastatic PCs with elevated TERT expression and using whole genome sequencing (WGS) identified genomic rearrangements that led to super-enhancer positioning proximal to the TERT promoter in two tumors. Materials and methods Patients and samples

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Hidewaki Nakagawa

a number of cancer genomes. GWAS, whole-genome sequencing (WGS), whole exome sequencing (WES), and RNA sequencing (RNA-Seq) have now been conducted for many types of cancer genomes worldwide, including the International Cancer Genome Consortium (ICGC

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Tirtha K Das and Ross L Cagan

Twenty-five years ago, RET was identified as the primary driver of multiple endocrine neoplasia type 2 (MEN2) syndrome. MEN2 is characterized by several transformation events including pheochromocytoma, parathyroid adenoma and, especially penetrant, medullary thyroid carcinoma (MTC). Overall, MTC is a rare but aggressive type of thyroid cancer for which no effective treatment currently exists. Surgery, radiation, radioisotope treatment and chemotherapeutics have all shown limited success, and none of these approaches have proven durable in advanced disease. Non-mammalian models that incorporate the oncogenic RET isoforms associated with MEN2 and other RET-associated diseases have been useful in delineating mechanisms underlying disease progression. These models have also identified novel targeted therapies as single agents and as combinations. These studies highlight the importance of modeling disease in the context of the whole animal, accounting for the complex interplay between tumor and normal cells in controlling disease progression as well as response to therapy. With convenient access to whole genome sequencing data from expanded thyroid cancer patient cohorts, non-mammalian models will become more complex, sophisticated and continue to complement future mammalian studies. In this review, we explore the contributions of non-mammalian models to our understanding of thyroid cancer including MTC, with a focus on Danio rerio and Drosophila melanogaster (fish and fly) models.

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Rodrigo A Toledo, Roxanne Hatakana, Delmar M Lourenço Jr, Susan C Lindsey, Cleber P Camacho, Marcio Almeida, José V Lima Jr, Tomoko Sekiya, Elena Garralda, Michel S Naslavsky, Guilherme L Yamamoto, Monize Lazar, Osorio Meirelles, Tiago J P Sobreira, Maria Lucia Lebrao, Yeda A O Duarte, John Blangero, Mayana Zatz, Janete M Cerutti, Rui M B Maciel and Sergio P A Toledo

sequencing (Applied Biosystems) was employed to sequence the reaction products, and the samples were run on an ABI Prism 3130xl – Genetic Analyzer (Applied Biosystems). Whole-exome and whole-genome sequencing Whole-exome sequence data were generated using

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

–15% of all sporadic PDAC ( Waddell et al. 2015 , Bailey et al. 2016 ). Indeed, a recent study on PDAC whole genome sequencing classified PDAC into ‘stable’, ‘locally rearranged’, ‘scattered’ and ‘unstable’ subtypes based on the variations in

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Jamie L Van Etten and Scott M Dehm

has provided evidence that primary tumors exhibit multiclonality coincident with multifocal disease. For example, whole-genome sequencing (WGS) in a cohort of five patients (Gleason scores 7–8) who underwent radical prostatectomies provided the first

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Vaishali I Parekh, Sita D Modali, James Welch, William F Simonds, Lee S Weinstein, Electron Kebebew and Sunita K Agarwal

). Whole genome sequencing (WGS) or whole exome sequencing (WES) of sporadic PNETs has revealed somatic MEN1 mutation in 37–44% of non-functioning PNETs ( Jiao et al . 2011 , Scarpa et al . 2017 ). However, four different WES studies of sporadic

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Paula Fontes Asprino, Rudinei Diogo Marques Linck, Jônatas Cesar, Florêncio Porto Freitas, Fernanda Christtanini Koyama, Rachel Simões Pimenta Riechelmann, Frederico Perego Costa, Paulo Marcelo Gehm Hoff, Pedro Alexandre Favoretto Galante, Diogo Meyer, Anamaria Aranha Camargo and Jorge Sabbaga

that examined whole-genome sequencing data from 98 pancreatic well-differentiated NENs described 5 patients (5.1%) carrying damaging rare germline variants in TSC2 ( Scarpa et al . 2017 ), providing an independent study consistent with our findings

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James F Powers, Brent Cochran, James D Baleja, Hadley D Sikes, Andrew D Pattison, Xue Zhang, Inna Lomakin, Annette Shepard-Barry, Karel Pacak, Sun Jin Moon, Troy F Langford, Kassi Taylor Stein, Richard W Tothill, Yingbin Ouyang and Arthur S Tischler

. Two cell lines, designated RS0 (for rat Sdhb null) and RS1/2 (for Sdhb haploinsufficient), originated from cultures of xenografts derived from two different primary tumors and maintained in 5% O 2 . Whole genome sequencing DNA extraction

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Willem E Corver, Joris Demmers, Jan Oosting, Shima Sahraeian, Arnoud Boot, Dina Ruano, Tom van Wezel and Hans Morreau

involved in metabolic switches. Possibly additional tumor drivers need to be identified. Indeed, we only found a PTEN- and a TP53 -inactivating gene variant after whole-genome sequencing (WGS) of three FTC-OV with NHG (data not shown). Thus, FTC-OV does