Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/176381
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dc.contributor.authorAvgustinova, Alexandra-
dc.contributor.authorSymeonidi, Aikaterini-
dc.contributor.authorCastellanos, Andrés-
dc.contributor.authorUrdiroz Urricelqui, Uxue-
dc.contributor.authorSolé Boldo, Llorenç-
dc.contributor.authorMartín, Mercè-
dc.contributor.authorPérez Rodríguez, Ivan-
dc.contributor.authorPrats, Neus-
dc.contributor.authorLehner, Ben-
dc.contributor.authorSupek, Fran-
dc.contributor.authorAznar Benitah, Salvador-
dc.date.accessioned2021-04-16T10:00:35Z-
dc.date.available2021-04-16T10:00:35Z-
dc.date.issued2018-01-01-
dc.identifier.issn1465-7392-
dc.identifier.urihttp://hdl.handle.net/2445/176381-
dc.description.abstractMutations in, and the altered expression of, epigenetic modifiers are pervasive in human tumours, making epigenetic factors attractive antitumour targets. The open-versus-closed chromatin state within the cells-of-origin of cancer correlates with the uneven distribution of mutations. However, the long-term effect of targeting epigenetic modifiers on mutability in patients with cancer is unclear. Here, we increased chromatin accessibility by deleting the histone H3 lysine 9 (H3K9) methyltransferase G9a in murine epidermis and show that this does not alter the single nucleotide variant burden or global genomic distribution in chemical mutagen-induced squamous tumours. G9a-depleted tumours develop after a prolonged latency compared with their wild-type counterparts, but are more aggressive and have an expanded cancer progenitor pool, pronounced genomic instability and frequent loss-of-function p53 mutations. Thus, we call for caution when assessing long-term therapeutic benefits of chromatin modifier inhibitors, which may promote more aggressive disease.-
dc.format.extent9-
dc.format.mimetypeapplication/pdf-
dc.language.isoeng-
dc.publisherNature Publishing Group-
dc.relation.isformatofversió postprint del document publicat a: https://doi.org/10.1038/s41556-018-0233-x-
dc.relation.ispartofNature Cell Biology, 2018, Vol. 20, num. 12, p. 1400-1409-
dc.relation.urihttps://doi.org/10.1038/s41556-018-0233-x-
dc.rights(c) Nature Publishing Group, 2018-
dc.subject.classificationEpigenètica-
dc.subject.classificationMetàstasi-
dc.subject.classificationCàncer de pell-
dc.subject.otherEpigenetics-
dc.subject.otherMetastasis-
dc.subject.otherSkin cancer-
dc.titleLoss of G9a preserves mutation patterns but increases chromatin accessibility, genomic instability and aggressiveness in skin tumours-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/AcceptedVersion-
dc.date.updated2021-04-16T09:52:24Z-
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/757700/EU//HYPER-INSIGHT-
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/787041/EU//LIPOMET-
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess-
dc.identifier.idimarina5610944-
dc.identifier.pmid30455462-
Appears in Collections:Articles publicats en revistes (Institut de Recerca Biomèdica (IRB Barcelona))

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