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dc.contributor.authorManners, Oliver
dc.contributor.authorMurphy, James
dc.contributor.authorColeman, Alex
dc.contributor.authorHughes, David J.
dc.contributor.authorWhitehouse, Adrian
dc.date.accessioned2018-10-03T16:30:07Z
dc.date.available2018-10-03T16:30:07Z
dc.date.issued2018-10
dc.identifier.citationManners , O , Murphy , J , Coleman , A , Hughes , D J & Whitehouse , A 2018 , ' Contribution of the KSHV and EBV lytic cycles to tumourigenesis ' , Current Opinion in Virology , vol. 32 , pp. 60-70 . https://doi.org/10.1016/j.coviro.2018.08.014en
dc.identifier.issn1879-6257
dc.identifier.otherPURE: 255853298
dc.identifier.otherPURE UUID: 9a3c5fc8-4cbd-4717-9022-8fa190f1aacb
dc.identifier.otherScopus: 85054017581
dc.identifier.otherWOS: 000452930300010
dc.identifier.urihttp://hdl.handle.net/10023/16138
dc.descriptionResearch in the Whitehouse laboratory is supported in parts by funding from Biotechnology and Biological Sciences Research Council (BB/M006557/1, BB/N014405/1), Medical Research Council (MR/R010145/1, 95505168), Worldwide Cancer Research (16-1025), Wellcome Trust (203826/Z/16/Z) and Rosetrees Trust (M662).en
dc.description.abstractKaposi’s Sarcoma-associated herpesvirus (KSHV) and Epstein Barr virus (EBV) are the causative agents of several malignancies. Like all herpesviruses, KSHV and EBV undergo distinct latent and lytic replication programmes. The transition between these states allows the establishment of a lifelong persistent infection, dissemination to sites of disease and the spread to new hosts. Latency-associated viral proteins have been well characterised in transformation and tumourigenesis pathways; however, a number of studies have shown that abrogation of KSHV and EBV lytic gene expression impairs the oncogenesis of several cancers. Furthermore, several lytically expressed proteins have been functionally tethered to the angioproliferative and anti-apoptotic phenotypes of virus-infected cells. As a result, the investigation and therapeutic targeting of KSHV and EBV lytic cycles may be essential for the treatment of their associated malignancies.
dc.language.isoeng
dc.relation.ispartofCurrent Opinion in Virologyen
dc.rightsCopyright © 2018 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).en
dc.subjectVirusen
dc.subjectOncogenic virusesen
dc.subjectLyticen
dc.subjectGammaherpesvirusen
dc.subjectKaposis-sarcomaen
dc.subjectQR355 Virologyen
dc.subjectRC0254 Neoplasms. Tumors. Oncology (including Cancer)en
dc.subject.lccQR355en
dc.subject.lccRC0254en
dc.titleContribution of the KSHV and EBV lytic cycles to tumourigenesisen
dc.typeJournal itemen
dc.description.versionPublisher PDFen
dc.contributor.institutionUniversity of St Andrews.Biomedical Sciences Research Complexen
dc.contributor.institutionUniversity of St Andrews.School of Biologyen
dc.identifier.doihttps://doi.org/10.1016/j.coviro.2018.08.014
dc.description.statusPeer revieweden
dc.identifier.urlhttps://authors.elsevier.com/sd/article/S1879625718300920en


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