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Whole-genome sequencing of nine esophageal adenocarcinoma cell lines

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Lynch_2016_F1000Res_CellLines_CC.pdf (1.492Mb)
Date
10/06/2016
Author
Contino, Gianmarco
Eldridge, Matthew D.
Secrier, Maria
Bower, Lawrence
Elliott, Rachael Fels
Weaver, Jamie
Lynch, Andy G.
Edwards, Paul A.W.
Fitzgerald, Rebecca C.
Keywords
R Medicine
QH301 Biology
QR180 Immunology
Medicine(all)
Immunology and Microbiology(all)
Biochemistry, Genetics and Molecular Biology(all)
Pharmacology, Toxicology and Pharmaceutics(all)
DAS
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Abstract
Esophageal adenocarcinoma (EAC) is highly mutated and molecularly heterogeneous. The number of cell lines available for study is limited and their genome has been only partially characterized. The availability of an accurate annotation of their mutational landscape is crucial for accurate experimental design and correct interpretation of genotype-phenotype findings. We performed high coverage, paired end whole genome sequencing on eight EAC cell lines-ESO26, ESO51, FLO-1, JH-EsoAd1, OACM5.1 C, OACP4 C, OE33, SK-GT-4-all verified against original patient material, and one esophageal high grade dysplasia cell line, CP-D. We have made available the aligned sequence data and report single nucleotide variants (SNVs), small insertions and deletions (indels), and copy number alterations, identified by comparison with the human reference genome and known single nucleotide polymorphisms (SNPs). We compare these putative mutations to mutations found in primary tissue EAC samples, to inform the use of these cell lines as a model of EAC.
Citation
Contino , G , Eldridge , M D , Secrier , M , Bower , L , Elliott , R F , Weaver , J , Lynch , A G , Edwards , P A W & Fitzgerald , R C 2016 , ' Whole-genome sequencing of nine esophageal adenocarcinoma cell lines ' , F1000Research , vol. 5 , 1336 . https://doi.org/10.12688/F1000RESEARCH.7033.1
Publication
F1000Research
Status
Peer reviewed
DOI
https://doi.org/10.12688/F1000RESEARCH.7033.1
ISSN
2046-1402
Type
Journal article
Rights
© 2016 Contino G et al. This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Description
This work was funded by an MRC Programme Grant to R.C.F. and a Cancer Research UK grant to PAWE. The pipeline for mutation calling is funded by Cancer Research UK as part of the International Cancer Genome Consortium. G.C. is a National Institute for Health Research Lecturer as part of a NIHR professorship grant to R.C.F. AGL is supported by a Cancer Research UK programme grant (C14303/A20406) to Simon Tavaré and the European Commission through the Horizon 2020 project SOUND (Grant Agreement no. 633974).
Collections
  • University of St Andrews Research
URI
http://hdl.handle.net/10023/11480

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