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dc.contributor.authorPitolli, Consueloen
dc.contributor.authorWang, Yingen
dc.contributor.authorMancini, Maraen
dc.contributor.authorShi, Yufangen
dc.contributor.authorAmelio, Ivanoen
dc.contributor.authorMelino, Gerryen
dc.date.accessioned2020-05-06T22:17:27Z
dc.date.available2020-05-06T22:17:27Z
dc.identifier.issn1422-0067
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/305053
dc.description.abstractThe key role of p53 as a tumor suppressor became clear when it was realized that this gene is mutated in 50% of human sporadic cancers and germline mutations expose to cancer along lifespan. Mutations in this gene not only abolish the tumor suppressive functions of p53 but also equip the protein with new pro-oncogenic functions. Here, we review the mechanisms by which these new functions gained by p53 mutants promote tumorigenesis.
dc.publisherMDPI AG
dc.rightsAttribution 4.0 International (CC BY)
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.titleDo mutations turn p53 into an oncogene?en
dc.typeArticle
prism.issueIdentifier24en
prism.number6241en
prism.publicationNameInternational Journal of Molecular Sciencesen
prism.volume20en
dc.identifier.doi10.17863/CAM.52135
dcterms.dateAccepted2019-12-05en
rioxxterms.versionofrecord10.3390/ijms20246241en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2019-12-05en
dc.contributor.orcidAmelio, Ivano [0000-0002-9126-5391]
dc.contributor.orcidMelino, Gerry [0000-0001-9428-5972]
dc.identifier.eissn1422-0067
rioxxterms.typeJournal Article/Reviewen
cam.issuedOnline2019-12-11en


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Attribution 4.0 International (CC BY)
Except where otherwise noted, this item's licence is described as Attribution 4.0 International (CC BY)