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dc.contributor.authorBailey, P.
dc.contributor.authorChang, D.
dc.contributor.authorNones, K.
dc.contributor.authorJohns, A.
dc.contributor.authorPatch, A.
dc.contributor.authorGingras, M.
dc.contributor.authorMiller, D.
dc.contributor.authorChrist, A.
dc.contributor.authorBruxner, T.
dc.contributor.authorQuinn, M.
dc.contributor.authorNourse, C.
dc.contributor.authorMurtaugh, L.
dc.contributor.authorHarliwong, I.
dc.contributor.authorIdrisoglu, S.
dc.contributor.authorManning, S.
dc.contributor.authorNourbakhsh, E.
dc.contributor.authorWani, S.
dc.contributor.authorFink, L.
dc.contributor.authorHolmes, O.
dc.contributor.authorChin, V.
dc.contributor.authorAnderson, M.
dc.contributor.authorKazakoff, S.
dc.contributor.authorLeonard, C.
dc.contributor.authorNewell, F.
dc.contributor.authorWaddell, N.
dc.contributor.authorWood, S.
dc.contributor.authorXu, Q.
dc.contributor.authorWilson, P.
dc.contributor.authorCloonan, N.
dc.contributor.authorKassahn, K.
dc.contributor.authorTaylor, D.
dc.contributor.authorQuek, K.
dc.contributor.authorRobertson, A.
dc.contributor.authorPantano, L.
dc.contributor.authorMincarelli, L.
dc.contributor.authorSanchez, L.
dc.contributor.authorEvers, L.
dc.contributor.authorWu, J.
dc.contributor.authorPinese, M.
dc.contributor.authorCowley, M.
dc.contributor.authorJones, M.
dc.contributor.authorColvin, E.
dc.contributor.authorNagrial, A.
dc.contributor.authorHumphrey, E.
dc.contributor.authorChantrill, L.
dc.contributor.authorMawson, A.
dc.contributor.authorHumphris, J.
dc.contributor.authorChou, A.
dc.contributor.authorPajic, M.
dc.contributor.authorScarlett, C.
dc.contributor.authorPinho, A.
dc.contributor.authorGiry-Laterriere, M.
dc.contributor.authorRooman, I.
dc.contributor.authorSamra, J.
dc.contributor.authorKench, J.
dc.contributor.authorLovell, J.
dc.contributor.authorMerrett, N.
dc.contributor.authorToon, C.
dc.contributor.authorEpari, K.
dc.contributor.authorNguyen, N.
dc.contributor.authorBarbour, A.
dc.contributor.authorZeps, Nikolajs
dc.contributor.authorMoran-Jones, K.
dc.contributor.authorJamieson, N.
dc.contributor.authorGraham, J.
dc.contributor.authorDuthie, F.
dc.contributor.authorOien, K.
dc.contributor.authorHair, J.
dc.contributor.authorGruetzmann, R.
dc.contributor.authorMaitra, A.
dc.contributor.authorIacobuzio-Donahue, C.
dc.contributor.authorWolfgang, C.
dc.contributor.authorMorgan, R.
dc.contributor.authorLawlor, R.
dc.contributor.authorCorbo, V.
dc.contributor.authorBassi, C.
dc.contributor.authorRusev, B.
dc.contributor.authorCapelli, P.
dc.contributor.authorSalvia, R.
dc.contributor.authorTortora, G.
dc.contributor.authorMukhopadhyay, D.
dc.contributor.authorPetersen, G.
dc.contributor.authorMunzy, D.
dc.contributor.authorFisher, W.
dc.contributor.authorKarim, S.
dc.contributor.authorEshleman, J.
dc.contributor.authorHruban, R.
dc.contributor.authorPilarsky, C.
dc.contributor.authorMorton, J.
dc.contributor.authorSansom, O.
dc.contributor.authorScarpa, A.
dc.contributor.authorMusgrove, E.
dc.contributor.authorBailey, U.
dc.contributor.authorHofmann, O.
dc.contributor.authorSutherland, R.
dc.contributor.authorWheeler, D.
dc.contributor.authorGill, A.
dc.contributor.authorGibbs, R.
dc.contributor.authorPearson, J.
dc.contributor.authorWaddell, N.
dc.contributor.authorBiankin, A.
dc.contributor.authorGrimmond, S.
dc.date.accessioned2018-04-30T02:40:25Z
dc.date.available2018-04-30T02:40:25Z
dc.date.created2018-04-16T07:41:32Z
dc.date.issued2016
dc.identifier.citationBailey, P. and Chang, D. and Nones, K. and Johns, A. and Patch, A. and Gingras, M. and Miller, D. et al. 2016. Genomic analyses identify molecular subtypes of pancreatic cancer. Nature. 531 (7592): pp. 47-52.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/66359
dc.identifier.doi10.1038/nature16965
dc.description.abstract

© 2016 Macmillan Publishers Limited. All rights reserved.Integrated genomic analysis of 456 pancreatic ductal adenocarcinomas identified 32 recurrently mutated genes that aggregate into 10 pathways: KRAS, TGF-β, WNT, NOTCH, ROBO/SLIT signalling, G1/S transition, SWI-SNF, chromatin modification, DNA repair and RNA processing. Expression analysis defined 4 subtypes: (1) squamous; (2) pancreatic progenitor; (3) immunogenic; and (4) aberrantly differentiated endocrine exocrine (ADEX) that correlate with histopathological characteristics. Squamous tumours are enriched for TP53 and KDM6A mutations, upregulation of the TP63ΔN transcriptional network, hypermethylation of pancreatic endodermal cell-fate determining genes and have a poor prognosis. Pancreatic progenitor tumours preferentially express genes involved in early pancreatic development (FOXA2/3, PDX1 and MNX1). ADEX tumours displayed upregulation of genes that regulate networks involved in KRAS activation, exocrine (NR5A2 and RBPJL), and endocrine differentiation (NEUROD1 and NKX2-2). Immunogenic tumours contained upregulated immune networks including pathways involved in acquired immune suppression. These data infer differences in the molecular evolution of pancreatic cancer subtypes and identify opportunities for therapeutic development.

dc.publisherNature Publishing Group
dc.titleGenomic analyses identify molecular subtypes of pancreatic cancer
dc.typeJournal Article
dcterms.source.volume531
dcterms.source.number7592
dcterms.source.startPage47
dcterms.source.endPage52
dcterms.source.issn0028-0836
dcterms.source.titleNature
curtin.accessStatusFulltext not available


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