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dc.contributor.authorMorris, MR
dc.contributor.authorRicketts, C
dc.contributor.authorGentle, D
dc.contributor.authorAbdulrahman, M
dc.contributor.authorClarke, N
dc.contributor.authorBrown, M
dc.contributor.authorKishida, T
dc.contributor.authorYao, M
dc.contributor.authorLatif, F
dc.contributor.authorMaher, ER
dc.date.accessioned2019-07-12T10:36:40Z
dc.date.available2019-07-12T10:36:40Z
dc.date.issued2010-02-15
dc.identifier.citationMorris, M. R., Ricketts, C., Gentle, D., Abdulrahman, M., Clarke, N., Brown, M., Kishida, T., Yao, M., Latif, F. and Maher, E. R. (2010) Identification of candidate tumour suppressor genes frequently methylated in renal cell carcinoma, Oncogene, 29, pp. 2104–2117.
dc.identifier.pmid20154727
dc.identifier.doi10.1038/onc.2009.493en
dc.identifier.urihttp://hdl.handle.net/2436/622545
dc.description.abstractPromoter region hyermethylation and transcriptional silencing is a frequent cause of tumour suppressor gene (TSG) inactivation in many types of human cancers. Functional epigenetic studies, in which gene expression is induced by treatment with demethylating agents, may identify novel genes with tumour-specific methylation. We used high-density gene expression microarrays in a functional epigenetic study of 11 renal cell carcinoma (RCC) cell lines. Twenty-eight genes were then selected for analysis of promoter methylation status in cell lines and primary RCC. Eight genes (BNC1, PDLIM4, RPRM, CST6, SFRP1, GREM1, COL14A1 and COL15A1) showed frequent (30% of RCC tested) tumour-specific promoter region methylation. Hypermethylation was associated with transcriptional silencing. Re-expression of BNC1, CST6, RPRM and SFRP1 suppressed the growth of RCC cell lines and RNA interference knock-down of BNC1, SFRP1 and COL14A1 increased the growth of RCC cell lines. Methylation of BNC1 or COL14A1 was associated with a poorer prognosis independent of tumour size, stage or grade. The identification of these epigenetically inactivated candidate RCC TSGs can provide insights into renal tumourigenesis and a basis for developing novel therapies and biomarkers for prognosis and detection. © 2010 Macmillan Publishers Limited.en
dc.formatapplication/PDFen
dc.languageeng
dc.language.isoenen
dc.publisherSpringer Natureen
dc.relation.urlhttps://www.nature.com/articles/onc2009493en
dc.subjectCell Line, Tumoren
dc.subjectHumansen
dc.subjectCarcinoma, Renal Cellen
dc.subjectOligonucleotide Array Sequence Analysisen
dc.subjectSurvival Analysisen
dc.subjectGene Expression Profilingen
dc.subjectCell Proliferationen
dc.subjectDNA Methylationen
dc.subjectEpigenesis, Geneticen
dc.subjectGene Silencingen
dc.subjectBase Sequenceen
dc.subjectGenes, Tumor Suppressoren
dc.subjectMolecular Sequence Dataen
dc.subjectAdulten
dc.subjectAgeden
dc.subjectMiddle Ageden
dc.subjectYoung Adulten
dc.titleIdentification of candidate tumour suppressor genes frequently methylated in renal cell carcinomaen
dc.typeJournal articleen
dc.identifier.eissn1476-5594
dc.identifier.journalOncogeneen
dc.date.updated2019-06-24T15:36:02Z
dc.contributor.institutionCancer Research UK Renal Molecular Oncology Group, University of Birmingham, Birmingham, UK.
pubs.place-of-publicationEngland
dc.date.accepted2009-11-22
rioxxterms.funderUniversity of Wolverhamptonen
rioxxterms.identifier.projectA5441en
rioxxterms.identifier.projectG0900871en
rioxxterms.versionAMen
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by-nc/4.0/en
rioxxterms.licenseref.startdate2019-07-12en
dc.source.volume29
dc.source.issue14
dc.source.beginpage2104
dc.source.endpage2117
dc.description.versionPublished version
refterms.dateFCD2019-07-12T10:36:30Z
refterms.versionFCDAM
refterms.dateFOA2019-07-12T10:36:40Z


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