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http://hdl.handle.net/2445/176381
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DC Field | Value | Language |
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dc.contributor.author | Avgustinova, Alexandra | - |
dc.contributor.author | Symeonidi, Aikaterini | - |
dc.contributor.author | Castellanos, Andrés | - |
dc.contributor.author | Urdiroz Urricelqui, Uxue | - |
dc.contributor.author | Solé Boldo, Llorenç | - |
dc.contributor.author | Martín, Mercè | - |
dc.contributor.author | Pérez Rodríguez, Ivan | - |
dc.contributor.author | Prats, Neus | - |
dc.contributor.author | Lehner, Ben | - |
dc.contributor.author | Supek, Fran | - |
dc.contributor.author | Aznar Benitah, Salvador | - |
dc.date.accessioned | 2021-04-16T10:00:35Z | - |
dc.date.available | 2021-04-16T10:00:35Z | - |
dc.date.issued | 2018-01-01 | - |
dc.identifier.issn | 1465-7392 | - |
dc.identifier.uri | http://hdl.handle.net/2445/176381 | - |
dc.description.abstract | Mutations 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.extent | 9 | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Nature Publishing Group | - |
dc.relation.isformatof | versió postprint del document publicat a: https://doi.org/10.1038/s41556-018-0233-x | - |
dc.relation.ispartof | Nature Cell Biology, 2018, Vol. 20, num. 12, p. 1400-1409 | - |
dc.relation.uri | https://doi.org/10.1038/s41556-018-0233-x | - |
dc.rights | (c) Nature Publishing Group, 2018 | - |
dc.source | Articles publicats en revistes (Institut de Recerca Biomèdica (IRB Barcelona)) | - |
dc.subject.classification | Epigenètica | - |
dc.subject.classification | Metàstasi | - |
dc.subject.classification | Càncer de pell | - |
dc.subject.other | Epigenetics | - |
dc.subject.other | Metastasis | - |
dc.subject.other | Skin cancer | - |
dc.title | Loss of G9a preserves mutation patterns but increases chromatin accessibility, genomic instability and aggressiveness in skin tumours | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/AcceptedVersion | - |
dc.date.updated | 2021-04-16T09:52:24Z | - |
dc.relation.projectID | info:eu-repo/grantAgreement/EC/H2020/757700/EU//HYPER-INSIGHT | - |
dc.relation.projectID | info:eu-repo/grantAgreement/EC/H2020/787041/EU//LIPOMET | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.idimarina | 5610944 | - |
dc.identifier.pmid | 30455462 | - |
Appears in Collections: | Articles publicats en revistes (Institut de Recerca Biomèdica (IRB Barcelona)) |
Files in This Item:
File | Description | Size | Format | |
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12541_5610944_nature_cell_saznar_fsupek.pdf | 16.16 MB | Adobe PDF | View/Open |
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