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dc.contributor.authorNik-Zainal, S
dc.contributor.authorDavies, H
dc.contributor.authorStaaf, J
dc.contributor.authorRamakrishna, M
dc.contributor.authorGlodzik, D
dc.contributor.authorZou, X
dc.contributor.authorMartincorena, I
dc.contributor.authorAlexandrov, LB
dc.contributor.authorMartin, S
dc.contributor.authorWedge, DC
dc.contributor.authorVan Loo, P
dc.contributor.authorJu, YS
dc.contributor.authorSmid, M
dc.contributor.authorBrinkman, AB
dc.contributor.authorMorganella, S
dc.contributor.authorAure, MR
dc.contributor.authorLingjærde, OC
dc.contributor.authorLangerød, A
dc.contributor.authorRingnér, M
dc.contributor.authorAhn, S-M
dc.contributor.authorBoyault, S
dc.contributor.authorBrock, JE
dc.contributor.authorBroeks, A
dc.contributor.authorButler, A
dc.contributor.authorDesmedt, C
dc.contributor.authorDirix, L
dc.contributor.authorDronov, S
dc.contributor.authorFatima, A
dc.contributor.authorFoekens, JA
dc.contributor.authorGerstung, M
dc.contributor.authorHooijer, GKJ
dc.contributor.authorJang, SJ
dc.contributor.authorJones, DR
dc.contributor.authorKim, H-Y
dc.contributor.authorKing, TA
dc.contributor.authorKrishnamurthy, S
dc.contributor.authorLee, HJ
dc.contributor.authorLee, J-Y
dc.contributor.authorLi, Y
dc.contributor.authorMcLaren, S
dc.contributor.authorMenzies, A
dc.contributor.authorMustonen, V
dc.contributor.authorO'Meara, S
dc.contributor.authorPauporté, I
dc.contributor.authorPivot, X
dc.contributor.authorPurdie, CA
dc.contributor.authorRaine, K
dc.contributor.authorRamakrishnan, K
dc.contributor.authorRodríguez-González, FG
dc.contributor.authorRomieu, G
dc.contributor.authorSieuwerts, AM
dc.contributor.authorSimpson, PT
dc.contributor.authorShepherd, R
dc.contributor.authorStebbings, L
dc.contributor.authorStefansson, OA
dc.contributor.authorTeague, J
dc.contributor.authorTommasi, S
dc.contributor.authorTreilleux, I
dc.contributor.authorVan den Eynden, GG
dc.contributor.authorVermeulen, P
dc.contributor.authorVincent-Salomon, A
dc.contributor.authorYates, L
dc.contributor.authorCaldas, C
dc.contributor.authorvan't Veer, L
dc.contributor.authorTutt, A
dc.contributor.authorKnappskog, S
dc.contributor.authorTan, BKT
dc.contributor.authorJonkers, J
dc.contributor.authorBorg, Å
dc.contributor.authorUeno, NT
dc.contributor.authorSotiriou, C
dc.contributor.authorViari, A
dc.contributor.authorFutreal, PA
dc.contributor.authorCampbell, PJ
dc.contributor.authorSpan, PN
dc.contributor.authorVan Laere, S
dc.contributor.authorLakhani, SR
dc.contributor.authorEyfjord, JE
dc.contributor.authorThompson, AM
dc.contributor.authorBirney, E
dc.contributor.authorStunnenberg, HG
dc.contributor.authorvan de Vijver, MJ
dc.contributor.authorMartens, JWM
dc.contributor.authorBørresen-Dale, A-L
dc.contributor.authorRichardson, AL
dc.contributor.authorKong, G
dc.contributor.authorThomas, G
dc.contributor.authorStratton, MR
dc.date.accessioned2017-03-24T14:55:51Z
dc.date.issued2016-06-02
dc.identifier.citationNature, 2016, 534 (7605), pp. 47 - 54
dc.identifier.issn0028-0836
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/518
dc.identifier.eissn1476-4687
dc.identifier.doi10.1038/nature17676
dc.description.abstractWe analysed whole-genome sequences of 560 breast cancers to advance understanding of the driver mutations conferring clonal advantage and the mutational processes generating somatic mutations. We found that 93 protein-coding cancer genes carried probable driver mutations. Some non-coding regions exhibited high mutation frequencies, but most have distinctive structural features probably causing elevated mutation rates and do not contain driver mutations. Mutational signature analysis was extended to genome rearrangements and revealed twelve base substitution and six rearrangement signatures. Three rearrangement signatures, characterized by tandem duplications or deletions, appear associated with defective homologous-recombination-based DNA repair: one with deficient BRCA1 function, another with deficient BRCA1 or BRCA2 function, the cause of the third is unknown. This analysis of all classes of somatic mutation across exons, introns and intergenic regions highlights the repertoire of cancer genes and mutational processes operating, and progresses towards a comprehensive account of the somatic genetic basis of breast cancer.
dc.formatPrint-Electronic
dc.format.extent47 - 54
dc.languageeng
dc.language.isoeng
dc.publisherNATURE PUBLISHING GROUP
dc.subjectHumans
dc.subjectBreast Neoplasms
dc.subjectDNA, Neoplasm
dc.subjectCohort Studies
dc.subjectDNA Mutational Analysis
dc.subjectGenomics
dc.subjectDNA Replication
dc.subjectMutagenesis
dc.subjectMutation
dc.subjectGenes, BRCA1
dc.subjectGenes, BRCA2
dc.subjectOncogenes
dc.subjectGenome, Human
dc.subjectFemale
dc.subjectMale
dc.subjectMutation Rate
dc.subjectRecombinational DNA Repair
dc.titleLandscape of somatic mutations in 560 breast cancer whole-genome sequences.
dc.typeJournal Article
dcterms.dateAccepted2016-03-17
rioxxterms.versionofrecord10.1038/nature17676
rioxxterms.licenseref.startdate2016-06
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfNature
pubs.issue7605
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR
pubs.publication-statusPublished
pubs.volume534
pubs.embargo.termsNot known
dc.contributor.icrauthorTutt, Andrew


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