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dc.contributor.authorYates, LRen_US
dc.contributor.authorKnappskog, Sen_US
dc.contributor.authorWedge, Den_US
dc.contributor.authorFarmery, JHRen_US
dc.contributor.authorGonzalez, Sen_US
dc.contributor.authorMartincorena, Ien_US
dc.contributor.authorAlexandrov, LBen_US
dc.contributor.authorVan Loo, Pen_US
dc.contributor.authorHaugland, HKen_US
dc.contributor.authorLilleng, PKen_US
dc.contributor.authorGundem, Gen_US
dc.contributor.authorGerstung, Men_US
dc.contributor.authorPappaemmanuil, Een_US
dc.contributor.authorGazinska, Pen_US
dc.contributor.authorBhosle, SGen_US
dc.contributor.authorJones, Den_US
dc.contributor.authorRaine, Ken_US
dc.contributor.authorMudie, Len_US
dc.contributor.authorLatimer, Cen_US
dc.contributor.authorSawyer, Een_US
dc.contributor.authorDesmedt, Cen_US
dc.contributor.authorSotiriou, Cen_US
dc.contributor.authorStratton, MRen_US
dc.contributor.authorSieuwerts, AMen_US
dc.contributor.authorLynch, AGen_US
dc.contributor.authorMartens, JWen_US
dc.contributor.authorRichardson, ALen_US
dc.contributor.authorTutt, Aen_US
dc.contributor.authorLønning, PEen_US
dc.contributor.authorCampbell, PJen_US
dc.date.accessioned2020-06-15T10:51:34Z
dc.date.issued2017-08en_US
dc.identifier.citationCancer cell, 2017, 32 (2), pp. 169 - 184.e7en_US
dc.identifier.issn1535-6108en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3742
dc.identifier.eissn1878-3686en_US
dc.identifier.doi10.1016/j.ccell.2017.07.005en_US
dc.description.abstractPatterns of genomic evolution between primary and metastatic breast cancer have not been studied in large numbers, despite patients with metastatic breast cancer having dismal survival. We sequenced whole genomes or a panel of 365 genes on 299 samples from 170 patients with locally relapsed or metastatic breast cancer. Several lines of analysis indicate that clones seeding metastasis or relapse disseminate late from primary tumors, but continue to acquire mutations, mostly accessing the same mutational processes active in the primary tumor. Most distant metastases acquired driver mutations not seen in the primary tumor, drawing from a wider repertoire of cancer genes than early drivers. These include a number of clinically actionable alterations and mutations inactivating SWI-SNF and JAK2-STAT3 pathways.en_US
dc.formatPrinten_US
dc.format.extent169 - 184.e7en_US
dc.languageengen_US
dc.language.isoengen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.subjectHumansen_US
dc.subjectBreast Neoplasmsen_US
dc.subjectNeoplasm Metastasisen_US
dc.subjectNeoplasm Recurrence, Localen_US
dc.subjectChromosomal Proteins, Non-Histoneen_US
dc.subjectTranscription Factorsen_US
dc.subjectEvolution, Molecularen_US
dc.subjectMutationen_US
dc.subjectAdulten_US
dc.subjectAgeden_US
dc.subjectAged, 80 and overen_US
dc.subjectMiddle Ageden_US
dc.subjectFemaleen_US
dc.subjectMaleen_US
dc.subjectSTAT3 Transcription Factoren_US
dc.subjectJanus Kinase 2en_US
dc.subjectBiomarkers, Tumoren_US
dc.titleGenomic Evolution of Breast Cancer Metastasis and Relapse.en_US
dc.typeJournal Article
dcterms.dateAccepted2017-07-14en_US
rioxxterms.versionofrecord10.1016/j.ccell.2017.07.005en_US
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0en_US
rioxxterms.licenseref.startdate2017-08en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfCancer cellen_US
pubs.issue2en_US
pubs.notesNot knownen_US
pubs.organisational-group/ICR
pubs.publication-statusPublisheden_US
pubs.volume32en_US
pubs.embargo.termsNot knownen_US
dc.contributor.icrauthorTutt, Andrewen_US


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