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dc.contributor.authorAlazawi, William*
dc.contributor.authorPett, Mark*
dc.contributor.authorArch, Barbara N.*
dc.contributor.authorScott, Laurie*
dc.contributor.authorFreeman, Tom*
dc.contributor.authorStanley, Margaret A.*
dc.contributor.authorColeman, Nicholas*
dc.date.accessioned2010-04-16T08:18:51Z
dc.date.available2010-04-16T08:18:51Z
dc.date.issued01/12/2002
dc.identifier.citationCancer Research, 62, 2002, pp. 6959-6965
dc.identifier.issn0008-5472en
dc.identifier.urihttp://hdl.handle.net/10034/96634
dc.descriptionThis article is not available through ChesterRep. It can be accessed at http://cancerres.aacrjournals.org/cgi/reprint/62/23/6959
dc.description.abstractEpisomal integration is a critical event in human papillomavirus (HPV)-related oncogenesis, although little information is currently available concerning the effect of integration on the host transcriptome. Expression microarrays were used to investigate the effect of integration of HPV16 on gene expression in cervical keratinocytes, using the unique cell line model W12. W12 was generated from a cervical low-grade squamous intraepithelial lesion "naturally" infected with HPV16 and at low passage contains approximately 100 HPV16 episomes/cell. With passage in vitro, integration of viral episomes is associated with the development of phenotypic and genomic abnormalities resembling those seen in cervical neoplastic progression in vivo. The Affymetrix U95A oligonucleotide array that contains probes for 12,600 human transcripts was used and 85 genes from a range of host cell pathways that show changes in expression levels after integration of HPV16 were identified. A range of genes not previously described as being involved in cervical neoplastic progression were identified. Interestingly, integration is associated with up-regulation of numerous IFN-responsive genes, in comparison with a baseline of episomally infected cells. These genes include p48, a component of the primary regulator of the IFN response pathway, IFN-stimulated gene factor 3. The physical state of high-risk HPV may substantially influence the response to IFN in infected keratinocytes.
dc.description.sponsorshipThis article was submitted to the RAE2008 for the University of Chester - Allied Health Professions and Studies.
dc.language.isoenen
dc.publisherAmerican Association for Cancer Research
dc.relation.urlhttp://cancerres.aacrjournals.orgen
dc.subjecthuman papillomavirus 16en
dc.titleChanges in cervical keratinocyte gene expression associated with integration of human papillomavirus 16en
dc.typeArticle
dc.contributor.departmentMedical Research Council Cancer Cell Unit, MRC/Hutchison Research Centre, Cambridge ; Department of Pathology, University of Cambridge ; Institute of Public Health, Cambridge ; Medical Research Council Human Genome Mapping Resource Centre, Cambridge ; Medical Research Council Human Genome Mapping Resource Centre, Cambridge ; Department of Pathology, University of Cambridge ; Medical Research Council Cancer Cell Unit, MRC/Hutchison Research Centre, Cambridge/Department of Pathology, University of Cambridge
dc.identifier.journalCancer Researchen
html.description.abstractEpisomal integration is a critical event in human papillomavirus (HPV)-related oncogenesis, although little information is currently available concerning the effect of integration on the host transcriptome. Expression microarrays were used to investigate the effect of integration of HPV16 on gene expression in cervical keratinocytes, using the unique cell line model W12. W12 was generated from a cervical low-grade squamous intraepithelial lesion "naturally" infected with HPV16 and at low passage contains approximately 100 HPV16 episomes/cell. With passage in vitro, integration of viral episomes is associated with the development of phenotypic and genomic abnormalities resembling those seen in cervical neoplastic progression in vivo. The Affymetrix U95A oligonucleotide array that contains probes for 12,600 human transcripts was used and 85 genes from a range of host cell pathways that show changes in expression levels after integration of HPV16 were identified. A range of genes not previously described as being involved in cervical neoplastic progression were identified. Interestingly, integration is associated with up-regulation of numerous IFN-responsive genes, in comparison with a baseline of episomally infected cells. These genes include p48, a component of the primary regulator of the IFN response pathway, IFN-stimulated gene factor 3. The physical state of high-risk HPV may substantially influence the response to IFN in infected keratinocytes.


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