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dc.contributor.authorAhmad, I
dc.contributor.authorSingh, LB
dc.contributor.authorYang, ZH
dc.contributor.authorKalna, G
dc.contributor.authorFleming, J
dc.contributor.authorFisher, G
dc.contributor.authorCooper, C
dc.contributor.authorCuzick, J
dc.contributor.authorBerney, DM
dc.contributor.authorMoller, H
dc.contributor.authorScardino, P
dc.contributor.authorLeung, HY
dc.contributor.authorGrp, TP
dc.date.accessioned2018-08-06T14:56:06Z
dc.date.issued2013-01-15
dc.identifier1
dc.identifier.citationBRITISH JOURNAL OF CANCER, 2013, 108 pp. 149 - 154
dc.identifier.issn0007-0920
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2277
dc.identifier.doi10.1038/bjc.2012.510
dc.description.abstractBackground: Aberrant mitogen/extracellular signal-regulated kinase 5 (MEK5)-extracellular signal-regulated protein kinase 5 (ERK5)-mediated signalling has been implicated in a number of tumour types including prostate cancer (CaP). The mechanism for ERK5 activation in CaP remains to be fully elucidated. Studies have recently implicated the role of microRNA (miRNA) mir143 expression in the regulation of ERK5 expression. Methods: We utilised a tissue microarray (TMA) of 530 CaP cores from 168 individual patients and stained for both mir143 and ERK5. These TMAs were scored by a combination of observer and automated methods. Results: We observed a strong inverse relation between ERK5 and mir143, which manifested itself most strongly in the subgroup of 417 cores with non-zero mir143 and ERK5 immunoreactivity, or with only one of mir143 or ERK5 being zero (cc = 0.2558 and P<0.0001). Mir143 neither correlate with Gleason scores or prostate-specific antigen levels, nor was it a predictor of disease-specific survival on univariate analysis. Conclusion: Although the mechanism for ERK5 activation in CaP remains to be fully elucidated, we have further validated the potential role of mir143 in regulating ERK5 levels in the clinical context. In addition, we demonstrate that the automated counting method for nuclear ERK5 is a clinically useful alterative to observer counting method in patient stratification in the context of ERK5 targeting therapy.
dc.format.extent149 - 154
dc.languageeng
dc.language.isoeng
dc.publisherNATURE PUBLISHING GROUP
dc.titleMir143 expression inversely correlates with nuclear ERK5 immunoreactivity in clinical prostate cancer
dc.typeJournal Article
rioxxterms.versionofrecord10.1038/bjc.2012.510
rioxxterms.licenseref.startdate2013-01-15
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfBRITISH JOURNAL OF CANCER
pubs.notesaffiliation: Leung, HY (Reprint Author), Beatson Inst Canc Res, Garscube Estate, Glasgow G61 1BD, Lanark, Scotland. Ahmad, I.; Singh, L. B.; Kalna, G.; Fleming, J.; Leung, H. Y., Beatson Inst Canc Res, Glasgow G61 1BD, Lanark, Scotland. Yang, Z. H.; Fisher, G.; Cuzick, J., Univ London, Ctr Canc Prevent, London EC1M 6BQ, England. Cooper, C., Inst Canc Res, Sutton SM2 5NG, Surrey, England. Berney, D. M., Univ London, Barts Canc Inst, Dept Mol Oncol, London EC1M 6BQ, England. Moller, H., Kings Coll London, Thames Canc Registry, London SE1 3QD, England. Scardino, P., Mem Sloan Kettering Canc Ctr, Dept Urol, New York, NY 10021 USA. keywords: mir143; ERK5; prostate cancer keywords-plus: MESSENGER-RNAS; BREAST-CANCER; MICRORNAS; MORTALITY; MIR-143; OVEREXPRESSION; PROMOTES; CELLS; KI-67 research-areas: Oncology web-of-science-categories: Oncology author-email: [email protected] orcid-numbers: Moller, Henrik/0000-0001-8200-5929 Leung, Hing Y./0000-0002-3933-3975 Berney, Daniel/0000-0001-5474-8696 funding-acknowledgement: Cancer Research UK; Medical Research Council funding-text: Cancer Research UK funded research work in the Urology Group, Beatson Institute for Cancer Research. IA was funded by a clinical research fellowship from the Medical Research Council and Cancer Research UK. We thank Clare Orange for technical assistance, and the ‘Think Pink’ charity for the purchase of the slide scanner. number-of-cited-references: 29 times-cited: 16 usage-count-last-180-days: 0 usage-count-since-2013: 6 journal-iso: Br. J. Cancer doc-delivery-number: 087YM unique-id: ISI:000314800600020 oa: gold_or_bronze da: 2018-08-06
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/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Cell Transformation
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.volume108
pubs.embargo.termsNot known
icr.researchteamCell Transformationen_US
dc.contributor.icrauthorCooper, Colinen


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