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dc.contributor.authorPaschalis, A
dc.contributor.authorSharp, A
dc.contributor.authorWelti, JC
dc.contributor.authorNeeb, A
dc.contributor.authorRaj, GV
dc.contributor.authorLuo, J
dc.contributor.authorPlymate, SR
dc.contributor.authorde Bono, JS
dc.date.accessioned2019-07-29T09:35:39Z
dc.date.issued2018-11
dc.identifier.citationNature reviews. Clinical oncology, 2018, 15 (11), pp. 663 - 675
dc.identifier.issn1759-4774
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3306
dc.identifier.eissn1759-4782
dc.identifier.doi10.1038/s41571-018-0085-0
dc.description.abstractAndrogen receptor (AR) splice variants (AR-Vs) have been implicated in the development and progression of metastatic prostate cancer. AR-Vs are truncated isoforms of the AR, a subset of which lack a ligand-binding domain and remain constitutively active in the absence of circulating androgens, thus promoting cancer cell proliferation. Consequently, AR-Vs have been proposed to contribute not only to resistance to anti-androgen therapies but also to resistance to radiotherapy in patients receiving combination therapy by promoting DNA repair. AR-Vs, such as AR-V7, have been associated with unfavourable clinical outcomes in patients; however, attempts to specifically inhibit or prevent the formation of AR-Vs have, to date, been unsuccessful. Thus, novel therapeutic strategies are desperately needed to address the oncogenic effects of AR-Vs, which can drive lethal forms of prostate cancer. Disruption of alternative splicing through modulation of the spliceosome is one such potential therapeutic avenue; however, our understanding of the biology of the spliceosome and how it contributes to prostate cancer remains incomplete, as reflected in the dearth of spliceosome-targeted therapeutic agents. In this Review, the authors outline the current understanding of the role of the spliceosome in the progression of prostate cancer and explore the therapeutic utility of manipulating alternative splicing to improve patient care.
dc.formatPrint
dc.format.extent663 - 675
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://www.rioxx.net/licenses/all-rights-reserved
dc.subjectSpliceosomes
dc.subjectHumans
dc.subjectProstatic Neoplasms
dc.subjectNeoplasm Metastasis
dc.subjectDisease Progression
dc.subjectProtein Isoforms
dc.subjectReceptors, Androgen
dc.subjectCell Proliferation
dc.subjectDNA Repair
dc.subjectAlternative Splicing
dc.subjectMale
dc.subjectCarcinogenesis
dc.titleAlternative splicing in prostate cancer.
dc.typeJournal Article
rioxxterms.versionofrecord10.1038/s41571-018-0085-0
rioxxterms.licenseref.urihttps://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2018-11
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfNature reviews. Clinical oncology
pubs.issue11
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Prostate Cancer Targeted Therapy Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Translational Therapeutics
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Prostate Cancer Targeted Therapy Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Translational Therapeutics
pubs.publication-statusPublished
pubs.volume15
pubs.embargo.termsNot known
icr.researchteamProstate Cancer Targeted Therapy Groupen_US
icr.researchteamTranslational Therapeuticsen_US
dc.contributor.icrauthorSharp, Adamen
dc.contributor.icrauthorDe Bono, Johannen


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