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dc.contributor.authorSoong, R.
dc.contributor.authorShah, N.
dc.contributor.authorPeh, B.
dc.contributor.authorChong, P.
dc.contributor.authorNg, S.
dc.contributor.authorZeps, Nikolajs
dc.contributor.authorJoseph, D.
dc.contributor.authorSalto-Tellez, M.
dc.contributor.authorIacopetta, B.
dc.contributor.authorIto, Y.
dc.date.accessioned2017-01-30T13:53:51Z
dc.date.available2017-01-30T13:53:51Z
dc.date.created2016-09-12T08:37:06Z
dc.date.issued2009
dc.identifier.citationSoong, R. and Shah, N. and Peh, B. and Chong, P. and Ng, S. and Zeps, N. and Joseph, D. et al. 2009. The expression of RUNX3 in colorectal cancer is associated with disease stage and patient outcome. British Journal of Cancer. 100 (5): pp. 676-679.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/36138
dc.identifier.doi10.1038/sj.bjc.6604899
dc.description.abstract

RUNX3 is believed to have tumour suppressor properties in several cancer types. Inactivation of RUNX3 has been shown to occur by methylation-induced transcriptional silencing and by mislocalization of the protein to the cytoplasm. The aim of this study was to examine the clinical significance of RUNX3 expression in a large series of colorectal cancers using immunohistochemistry and tissue arrays. With advancing tumour stage, expression of RUNX3 in the nucleus decreased, whereas expression restricted to the cytoplasmic compartment increased. Nuclear RUNX3 expression was associated with significantly better patient survival compared to tumours in which the expression of RUNX3 was restricted to the cytoplasm (P=0.025). These results support a role for RUNX3 as a tumour suppressor in colorectal cancer. © 2009 Cancer Research UK.

dc.publisherNature Publishing Group
dc.titleThe expression of RUNX3 in colorectal cancer is associated with disease stage and patient outcome
dc.typeJournal Article
dcterms.source.volume100
dcterms.source.number5
dcterms.source.startPage676
dcterms.source.endPage679
dcterms.source.issn0007-0920
dcterms.source.titleBritish Journal of Cancer
curtin.accessStatusOpen access via publisher


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