Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/102320
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dc.contributor.authorWaddell, N.en
dc.contributor.authorPajic, M.en
dc.contributor.authorPatch, A.en
dc.contributor.authorChang, D.en
dc.contributor.authorKassahn, K.en
dc.contributor.authorBailey, P.en
dc.contributor.authorJohns, A.en
dc.contributor.authorMiller, D.en
dc.contributor.authorNones, K.en
dc.contributor.authorQuek, K.en
dc.contributor.authorQuinn, M.en
dc.contributor.authorRobertson, A.en
dc.contributor.authorFadlullah, M.en
dc.contributor.authorBruxner, T.en
dc.contributor.authorChrist, A.en
dc.contributor.authorHarliwong, I.en
dc.contributor.authorIdrisoglu, S.en
dc.contributor.authorManning, S.en
dc.contributor.authorNourse, C.en
dc.contributor.authorNourbakhsh, E.en
dc.contributor.authoret al.en
dc.date.issued2015en
dc.identifier.citationNature, 2015; 518(7540):495-501en
dc.identifier.issn0028-0836en
dc.identifier.issn1476-4687en
dc.identifier.urihttp://hdl.handle.net/2440/102320-
dc.descriptionPublished online 25 February 2015en
dc.description.abstractPancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded.en
dc.description.statementofresponsibilityNicola Waddell ... Karin S. Kassahn ... Nam Q. Nguyen ... et al. (Australian Pancreatic Cancer Genome Initiative)en
dc.language.isoenen
dc.publisherNature Publishing Groupen
dc.rights©2015 Macmillan Publishers Limited. All rights reserveden
dc.subjectAustralian Pancreatic Cancer Genome Initiativeen
dc.titleWhole genomes redefine the mutational landscape of pancreatic canceren
dc.typeJournal articleen
dc.identifier.rmid0030035702en
dc.identifier.doi10.1038/nature14169en
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/631701en
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/535903en
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/427601en
dc.identifier.pubid177636-
pubs.library.collectionMedicine publicationsen
pubs.library.teamDS03en
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
Appears in Collections:Medicine publications

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