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dc.contributor.authorCooper, CSen_US
dc.contributor.authorFoster, CSen_US
dc.date.accessioned2018-08-30T13:47:38Z
dc.date.issued2009-01-22en_US
dc.identifier2en_US
dc.identifier.citationBRITISH JOURNAL OF CANCER, 2009, 100 pp. 240 - 245en_US
dc.identifier.issn0007-0920en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2452
dc.identifier.doi10.1038/sj.bjc.6604771en_US
dc.description.abstractSubstantial evidence now supports the view that epigenetic changes have a role in the development of human prostate cancer. Analyses of the patterns of epigenetic alteration are providing important insights into the origin of this disease and have identified specific alterations that may serve as useful diagnostic and prognostic biomarkers. Examination of cancer methylation patterns supports a stem cell origin of prostate cancer. It is well established that methylation of GSTpi is a marker of prostate cancer, and global patterns of histone marking appear to be linked to cancer prognosis with levels of acetylated histones H3K9, H3K18, and H4K12, and of dimethylated H4R3 and H3K4, dividing low-grade prostate cancer (Gleason 6 or less) into two prognostically separate groups. Elevated levels of several components of the polycomb group protein complex, EZH2, BMI1, and RING1, can also act as biomarkers of poor clinical outcome. Many components of the epigenetic machinery, including histone deacetylase (whose expression level is linked to the TMPRSS2: ERG translocation) and the histone methylase EZH2, are potential therapeutic targets. The recent discovery of the role of small RNAs in governing the epigenetic status of individual genes offers exciting new possibilities in therapeutics and chemoprevention.en_US
dc.format.extent240 - 245en_US
dc.languageEnglishen_US
dc.language.isoEnglishen_US
dc.publisherNATURE PUBLISHING GROUPen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.titleConcepts of epigenetics in prostate cancer developmenten_US
dc.typeJournal Article
rioxxterms.versionofrecord10.1038/sj.bjc.6604771en_US
rioxxterms.licenseref.startdate2009-01-22en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfBRITISH JOURNAL OF CANCERen_US
pubs.notesaffiliation: Cooper, CS (Reprint Author), Inst Canc Res, Male Urol Canc Res Ctr, 15 Cotswold Rd, Sutton SM2 5NG, Surrey, England. Cooper, C. S., Inst Canc Res, Male Urol Canc Res Ctr, Sutton SM2 5NG, Surrey, England. Foster, C. S., Univ Liverpool, Div Cellular Pathol & Mol Genet, Liverpool L69 3GA, Merseyside, England. keywords: epigenetic; prostate cancer; histone marks; DNA methylation; stem cells; small RNAs keywords-plus: DNA METHYLATION; PROMOTER METHYLATION; DOWN-REGULATION; HUMAN-CELLS; CPG ISLAND; GENE; HYPERMETHYLATION; PATTERNS; EZH2; RNA research-areas: Oncology web-of-science-categories: Oncology author-email: colin.cooper@icr.ac.uk funding-acknowledgement: Grand Charity of Freemasons; Medical Research Council [G0501019] funding-text: Colin Cooper is funded by the Grand Charity of Freemasons, Professor of Molecular Biology at the Institute of Cancer Research. Chris Foster is the George Holt Professor of Pathology at the University of Liverpool. We thank Christine Bell for typing the manuscript and Sandra Edwards for preparing the figures. number-of-cited-references: 31 times-cited: 64 usage-count-last-180-days: 0 usage-count-since-2013: 12 journal-iso: Br. J. Cancer doc-delivery-number: 397BV unique-id: ISI:000262637800004 oa: gold_or_bronze da: 2018-08-29en_US
pubs.notesNot knownen_US
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/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Cell Transformation
pubs.volume100en_US
pubs.embargo.termsNot knownen_US
icr.researchteamCell Transformationen_US
dc.contributor.icrauthorCooper, Colinen_US


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