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Article: Epigenetic and genetic alterations of p33 ING1b in ovarian cancer

TitleEpigenetic and genetic alterations of p33 ING1b in ovarian cancer
Authors
Issue Date2005
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2005, v. 26 n. 4, p. 855-863 How to Cite?
Abstractp33 ING1b is a candidate tumor suppressor gene and a nuclear protein. We investigated whether genetic and epigenetic mechanisms affect p33 ING1b expression in ovarian cancer thus contributing toward its pathogenesis. A total of 111 ovarian cancers collected from Beijing and Hong Kong were used for this study. Weak or negative p33 ING1b protein expression was demonstrated by immunohistochemistry on tissue microarray in 28/111 cases. Real-time quantitative RT-PCR also showed overall significant reduction of p33 ING1b mRNA expression (P = 0.0137), with 53.1% (17/32) cases showing 2- to 5-fold reduction and absence of expression. The reduction of mRNA expression in cancer correlated with decreased p33 ING1b protein expression (P < 0.0001). While no p33 ING1b mutation was found, allelic loss at the p33 ING1b locus was demonstrated in 25% (8/32) cases. The allelic loss profiles also showed statistical significant correlation with reduction of p33 ING1b protein and mRNA expression (P = 0.031 and 0.030). Promoter methylation as assessed by methylation specific PCR was found in 23.9% (21/88) cases analyzed. Bisulfite sequencing results confirmed the p33 ING1b promoter methylation status of these methylation positive cases. Statistical significant correlation between methylation and mRNA expression (P = 0.006) was demonstrated. Treatment with demethylating drug, 5′-aza-2′- deoxycytidine, resulted in dosage-dependent elevated mRNA expression of p33 ING1b in ovarian cancer cell lines. This is the first study reporting epigenetic mechanism regulating the p33 ING1b expression. Our findings support that genetic and epigenetic alteration of p33 ING1b are likely to contribute towards the pathogenesis of ovarian cancers. © Oxford University Press 2005; all rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/87048
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShen, DHen_HK
dc.contributor.authorChan, KYKen_HK
dc.contributor.authorKhoo, USen_HK
dc.contributor.authorNgan, HYSen_HK
dc.contributor.authorXue, WCen_HK
dc.contributor.authorChiu, PMen_HK
dc.contributor.authorIp, Pen_HK
dc.contributor.authorCheung, ANYen_HK
dc.date.accessioned2010-09-06T09:24:38Z-
dc.date.available2010-09-06T09:24:38Z-
dc.date.issued2005en_HK
dc.identifier.citationCarcinogenesis, 2005, v. 26 n. 4, p. 855-863en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/87048-
dc.description.abstractp33 ING1b is a candidate tumor suppressor gene and a nuclear protein. We investigated whether genetic and epigenetic mechanisms affect p33 ING1b expression in ovarian cancer thus contributing toward its pathogenesis. A total of 111 ovarian cancers collected from Beijing and Hong Kong were used for this study. Weak or negative p33 ING1b protein expression was demonstrated by immunohistochemistry on tissue microarray in 28/111 cases. Real-time quantitative RT-PCR also showed overall significant reduction of p33 ING1b mRNA expression (P = 0.0137), with 53.1% (17/32) cases showing 2- to 5-fold reduction and absence of expression. The reduction of mRNA expression in cancer correlated with decreased p33 ING1b protein expression (P < 0.0001). While no p33 ING1b mutation was found, allelic loss at the p33 ING1b locus was demonstrated in 25% (8/32) cases. The allelic loss profiles also showed statistical significant correlation with reduction of p33 ING1b protein and mRNA expression (P = 0.031 and 0.030). Promoter methylation as assessed by methylation specific PCR was found in 23.9% (21/88) cases analyzed. Bisulfite sequencing results confirmed the p33 ING1b promoter methylation status of these methylation positive cases. Statistical significant correlation between methylation and mRNA expression (P = 0.006) was demonstrated. Treatment with demethylating drug, 5′-aza-2′- deoxycytidine, resulted in dosage-dependent elevated mRNA expression of p33 ING1b in ovarian cancer cell lines. This is the first study reporting epigenetic mechanism regulating the p33 ING1b expression. Our findings support that genetic and epigenetic alteration of p33 ING1b are likely to contribute towards the pathogenesis of ovarian cancers. © Oxford University Press 2005; all rights reserved.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.rightsCarcinogenesis . Copyright © Oxford University Press.en_HK
dc.subject.meshAdenocarcinoma, Clear Cell - genetics - metabolism - pathologyen_HK
dc.subject.meshAntimetabolites, Antineoplastic - pharmacologyen_HK
dc.subject.meshAzacitidine - analogs & derivatives - pharmacologyen_HK
dc.subject.meshCarcinoma, Endometrioid - genetics - metabolism - pathologyen_HK
dc.subject.meshCase-Control Studiesen_HK
dc.subject.meshCell Cycle Proteinsen_HK
dc.subject.meshCpG Islandsen_HK
dc.subject.meshCystadenocarcinoma, Mucinous - genetics - metabolism - pathologyen_HK
dc.subject.meshCystadenocarcinoma, Serous - genetics - metabolism - pathologyen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshDNA-Binding Proteinsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshGenes, Tumor Suppressoren_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunoenzyme Techniquesen_HK
dc.subject.meshIntracellular Signaling Peptides and Proteinsen_HK
dc.subject.meshLoss of Heterozygosityen_HK
dc.subject.meshMutation - geneticsen_HK
dc.subject.meshNuclear Proteinsen_HK
dc.subject.meshOvarian Neoplasms - genetics - metabolism - pathologyen_HK
dc.subject.meshOvary - metabolism - pathologyen_HK
dc.subject.meshPromoter Regions, Genetic - geneticsen_HK
dc.subject.meshProteins - geneticsen_HK
dc.subject.meshRNA, Messenger - genetics - metabolismen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.subject.meshTumor Suppressor Proteinsen_HK
dc.titleEpigenetic and genetic alterations of p33 ING1b in ovarian canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-3334&volume=26&spage=855&epage=63&date=2005&atitle=Epigenetic+and+genetic+alterations+of+p33ING1b+in+ovarian+cancer.en_HK
dc.identifier.emailChan, KYK: kelvinc@pathology.hku.hken_HK
dc.identifier.emailKhoo, US: uskhoo@hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.emailCheung, ANY: anycheun@hkucc.hku.hken_HK
dc.identifier.authorityChan, KYK=rp00453en_HK
dc.identifier.authorityKhoo, US=rp00362en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/carcin/bgi011en_HK
dc.identifier.pmid15677627-
dc.identifier.scopuseid_2-s2.0-17844395211en_HK
dc.identifier.hkuros101218en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-17844395211&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume26en_HK
dc.identifier.issue4en_HK
dc.identifier.spage855en_HK
dc.identifier.epage863en_HK
dc.identifier.isiWOS:000227976700018-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridShen, DH=7401738584en_HK
dc.identifier.scopusauthoridChan, KYK=7406034195en_HK
dc.identifier.scopusauthoridKhoo, US=7004195799en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.scopusauthoridXue, WC=7103165268en_HK
dc.identifier.scopusauthoridChiu, PM=7103182596en_HK
dc.identifier.scopusauthoridIp, P=7003622683en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK
dc.identifier.citeulike140066-

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