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Article: Expression of cytoplasmic and nuclear Survivin in primary and secondary human glioblastoma

TitleExpression of cytoplasmic and nuclear Survivin in primary and secondary human glioblastoma
Authors
Issue Date2006
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjc
Citation
British Journal Of Cancer, 2006, v. 94 n. 1, p. 108-114 How to Cite?
AbstractClinically, human glioblastoma (GBM) may develop de novo or from a low-grade glioma (secondary GBM), and molecular alterations in the two pathways may differ. This study examined the status of Survivin expression and apoptosis in 30 primary and 26 secondary GBMs. Our results show that cytoplasmic Survivin positivity was significantly (P < 0.001) more frequent in primary GBMs (83%) than that in secondary GBMs (46%). In addition, an inverse correlation of cytoplasmc Survivin positivity with GBM apoptotic index, and a positive association between cytoplasmic Survivin and size of the tumours were observed. These results suggest that cytoplasmic Survivin, via its antiapoptotic function, may be involved in the tumorigenesis of many primary GBMs, but only in a small fraction of secondary GBMs. Furthermore, the overall progression times from low-grade precursor lesions to secondary GBMs were significantly shorter (P < 0.05) in cytoplasmic Survivin-positive cases (mean, 15.6 months) than those in Survivin-negative cases (mean, 23.8 moths), and the positive expression level of Survivin in cytoplasm was upregulated in most secondary GBMs when compared to matched pre-existing low-graded lesions. These results suggest that the increased accumulation of Survivin in the cytoplasm of more malignant glioma cells may prove to be a selective advantage, thus accelerating progression to a more aggressive phenotype. © 2006 Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/71950
ISSN
2015 Impact Factor: 5.569
2015 SCImago Journal Rankings: 2.939
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXie, Den_HK
dc.contributor.authorZeng, YXen_HK
dc.contributor.authorWang, HJen_HK
dc.contributor.authorWen, JMen_HK
dc.contributor.authorTao, Yen_HK
dc.contributor.authorSham, JSTen_HK
dc.contributor.authorGuan, XYen_HK
dc.date.accessioned2010-09-06T06:36:49Z-
dc.date.available2010-09-06T06:36:49Z-
dc.date.issued2006en_HK
dc.identifier.citationBritish Journal Of Cancer, 2006, v. 94 n. 1, p. 108-114en_HK
dc.identifier.issn0007-0920en_HK
dc.identifier.urihttp://hdl.handle.net/10722/71950-
dc.description.abstractClinically, human glioblastoma (GBM) may develop de novo or from a low-grade glioma (secondary GBM), and molecular alterations in the two pathways may differ. This study examined the status of Survivin expression and apoptosis in 30 primary and 26 secondary GBMs. Our results show that cytoplasmic Survivin positivity was significantly (P < 0.001) more frequent in primary GBMs (83%) than that in secondary GBMs (46%). In addition, an inverse correlation of cytoplasmc Survivin positivity with GBM apoptotic index, and a positive association between cytoplasmic Survivin and size of the tumours were observed. These results suggest that cytoplasmic Survivin, via its antiapoptotic function, may be involved in the tumorigenesis of many primary GBMs, but only in a small fraction of secondary GBMs. Furthermore, the overall progression times from low-grade precursor lesions to secondary GBMs were significantly shorter (P < 0.05) in cytoplasmic Survivin-positive cases (mean, 15.6 months) than those in Survivin-negative cases (mean, 23.8 moths), and the positive expression level of Survivin in cytoplasm was upregulated in most secondary GBMs when compared to matched pre-existing low-graded lesions. These results suggest that the increased accumulation of Survivin in the cytoplasm of more malignant glioma cells may prove to be a selective advantage, thus accelerating progression to a more aggressive phenotype. © 2006 Cancer Research.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjcen_HK
dc.relation.ispartofBritish Journal of Canceren_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshBrain Neoplasms - genetics - physiopathology - secondaryen_HK
dc.subject.meshCell Transformation, Neoplasticen_HK
dc.subject.meshChilden_HK
dc.subject.meshDisease Progressionen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Profilingen_HK
dc.subject.meshGlioblastoma - genetics - physiopathology - secondaryen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshInhibitor of Apoptosis Proteinsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMicrotubule-Associated Proteins - biosynthesisen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshNeoplasm Proteins - biosynthesisen_HK
dc.subject.meshPhenotypeen_HK
dc.subject.meshPrognosisen_HK
dc.titleExpression of cytoplasmic and nuclear Survivin in primary and secondary human glioblastomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-0920&volume=94&spage=108&epage=114&date=2006&atitle=Expression+of+cytoplasmic+and+nuclear+Survivin+in+primary+and+secondary+human+glioblastoma.en_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.bjc.6602904en_HK
dc.identifier.pmid16404364en_HK
dc.identifier.scopuseid_2-s2.0-30644472260en_HK
dc.identifier.hkuros119645en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-30644472260&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume94en_HK
dc.identifier.issue1en_HK
dc.identifier.spage108en_HK
dc.identifier.epage114en_HK
dc.identifier.isiWOS:000234556100018-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridXie, D=35070710200en_HK
dc.identifier.scopusauthoridZeng, YX=7402981579en_HK
dc.identifier.scopusauthoridWang, HJ=8941461500en_HK
dc.identifier.scopusauthoridWen, JM=7402701931en_HK
dc.identifier.scopusauthoridTao, Y=36121574400en_HK
dc.identifier.scopusauthoridSham, JST=7101655565en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.citeulike438072-

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