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dc.contributor.authorVerschuren, Emmy W
dc.contributor.authorKlefstrom, Juha
dc.contributor.authorEvan, Gerard I
dc.contributor.authorJones, Nic
dc.date.accessioned2009-10-12T12:16:45Z
dc.date.available2009-10-12T12:16:45Z
dc.date.issued2002-09
dc.identifier.citationThe oncogenic potential of Kaposi's sarcoma-associated herpesvirus cyclin is exposed by p53 loss in vitro and in vivo. 2002, 2 (3):229-41 Cancer Cellen
dc.identifier.issn1535-6108
dc.identifier.pmid12242155
dc.identifier.doihttp://dx.doi.org/10.1016/S1535-6108(02)00123-X
dc.identifier.urihttp://hdl.handle.net/10541/84045
dc.description.abstractExpression of the Kaposi's sarcoma-associated herpesvirus (KSHV) cyclin D homolog, K cyclin, is thought to contribute to viral oncogenesis. We show that K cyclin expression in primary cells sensitizes to apoptosis and induces growth arrest, both of which are dependent on p53 but independent of E2F1 or p19(ARF). DNA synthesis, but not cytokinesis, continues in K cyclin-expressing cells, leading to multinucleation and polyploidy. Such polyploid cells exhibit pronounced centrosome amplification and consequent aneuploidy. Our data suggest that K cyclin expression leads to cytokinesis defects and polyploidy, which activates p53. However, in the absence of p53, such cells survive and expand as an aneuploid population. Corroborating these findings, in vivo Emu; K cyclin expression cooperates with p53 loss in the induction of lymphomas.
dc.language.isoenen
dc.subject.meshAnimals
dc.subject.meshApoptosis
dc.subject.meshCell Division
dc.subject.meshCells, Cultured
dc.subject.meshCentrosome
dc.subject.meshCyclins
dc.subject.meshEmbryo, Mammalian
dc.subject.meshFibroblasts
dc.subject.meshGenes, p53
dc.subject.meshHerpesvirus 8, Human
dc.subject.meshHumans
dc.subject.meshLymphoma
dc.subject.meshMice
dc.subject.meshMice, Transgenic
dc.subject.meshPolyploidy
dc.subject.meshSarcoma, Kaposi
dc.subject.meshTransduction, Genetic
dc.titleThe oncogenic potential of Kaposi's sarcoma-associated herpesvirus cyclin is exposed by p53 loss in vitro and in vivo.en
dc.typeArticleen
dc.contributor.departmentCancer Research Institute, University of California, San Francisco, San Francisco, CA 94115, USA.en
dc.identifier.journalCancer Cellen
html.description.abstractExpression of the Kaposi's sarcoma-associated herpesvirus (KSHV) cyclin D homolog, K cyclin, is thought to contribute to viral oncogenesis. We show that K cyclin expression in primary cells sensitizes to apoptosis and induces growth arrest, both of which are dependent on p53 but independent of E2F1 or p19(ARF). DNA synthesis, but not cytokinesis, continues in K cyclin-expressing cells, leading to multinucleation and polyploidy. Such polyploid cells exhibit pronounced centrosome amplification and consequent aneuploidy. Our data suggest that K cyclin expression leads to cytokinesis defects and polyploidy, which activates p53. However, in the absence of p53, such cells survive and expand as an aneuploid population. Corroborating these findings, in vivo Emu; K cyclin expression cooperates with p53 loss in the induction of lymphomas.


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