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Article: Methylation profile in benign, borderline and malignant ovarian tumors

TitleMethylation profile in benign, borderline and malignant ovarian tumors
Authors
KeywordsConcurrent methylation
Methylation profile
Ovarian tumors
Tumor suppressor genes
Issue Date2007
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00432/index.htm
Citation
Journal Of Cancer Research And Clinical Oncology, 2007, v. 133 n. 5, p. 331-341 How to Cite?
AbstractPurpose: Promoter hypermethylation is a common phenomenon in neoplasm. The aims of this study were (a) to compare the methylation profiles in different types of ovarian tumors and (b) to determine the possible relationship between the methylation status and different clinicopathologic characteristics. Methods: We examined the promoter methylation status of 9 tumor suppressor genes (RARβ2, TMS1, RIZ1, P15, P16, PTEN, MINT31, APC and HIC1) in 89 ovarian cancers, 16 borderline ovarian tumors, 19 benign ovarian tumors, 16 normal ovarian tissue and 5 ovarian cancer cell lines. The methylation status was examined with respect to clinicopathologic characteristics of the ovarian cancer patients. Results: Methylation indices for ovarian cancer, borderline ovarian tumor, benign ovarian tumor, normal ovarian tissue and ovarian cancer cell lines were 28.8, 20.1, 10.5, 11.8 and 42.2%, respectively. It was significantly higher in ovarian cancer, borderline ovarian tumor and ovarian cancer cell lines (X 2 test, P < 0.001, P = 0.01 and P < 0.001, respectively) than benign or normal ovarian tissues. In ovarian cancer, concurrent methylation of at least two genes (CM2) was associated with early stage disease (X 2 test, P = 0.035) and less recurrence (X 2 test, P = 0.020). When the methylation statuses of the nine genes as well as CM2 were included in multivariate Cox Regression analysis, CM2 was the only independent predictor for survival (P = 0.013). Conclusion: CM2 was an independent predictor for survival in ovarian cancer. © 2006 Springer-Verlag.
Persistent Identifierhttp://hdl.handle.net/10722/87409
ISSN
2015 Impact Factor: 3.141
2015 SCImago Journal Rankings: 1.190
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTam, KFen_HK
dc.contributor.authorLiu, VWSen_HK
dc.contributor.authorLiu, SSen_HK
dc.contributor.authorTsang, PCKen_HK
dc.contributor.authorCheung, ANYen_HK
dc.contributor.authorYip, AMWen_HK
dc.contributor.authorNgan, HYSen_HK
dc.date.accessioned2010-09-06T09:29:18Z-
dc.date.available2010-09-06T09:29:18Z-
dc.date.issued2007en_HK
dc.identifier.citationJournal Of Cancer Research And Clinical Oncology, 2007, v. 133 n. 5, p. 331-341en_HK
dc.identifier.issn0171-5216en_HK
dc.identifier.urihttp://hdl.handle.net/10722/87409-
dc.description.abstractPurpose: Promoter hypermethylation is a common phenomenon in neoplasm. The aims of this study were (a) to compare the methylation profiles in different types of ovarian tumors and (b) to determine the possible relationship between the methylation status and different clinicopathologic characteristics. Methods: We examined the promoter methylation status of 9 tumor suppressor genes (RARβ2, TMS1, RIZ1, P15, P16, PTEN, MINT31, APC and HIC1) in 89 ovarian cancers, 16 borderline ovarian tumors, 19 benign ovarian tumors, 16 normal ovarian tissue and 5 ovarian cancer cell lines. The methylation status was examined with respect to clinicopathologic characteristics of the ovarian cancer patients. Results: Methylation indices for ovarian cancer, borderline ovarian tumor, benign ovarian tumor, normal ovarian tissue and ovarian cancer cell lines were 28.8, 20.1, 10.5, 11.8 and 42.2%, respectively. It was significantly higher in ovarian cancer, borderline ovarian tumor and ovarian cancer cell lines (X 2 test, P < 0.001, P = 0.01 and P < 0.001, respectively) than benign or normal ovarian tissues. In ovarian cancer, concurrent methylation of at least two genes (CM2) was associated with early stage disease (X 2 test, P = 0.035) and less recurrence (X 2 test, P = 0.020). When the methylation statuses of the nine genes as well as CM2 were included in multivariate Cox Regression analysis, CM2 was the only independent predictor for survival (P = 0.013). Conclusion: CM2 was an independent predictor for survival in ovarian cancer. © 2006 Springer-Verlag.en_HK
dc.languageengen_HK
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00432/index.htmen_HK
dc.relation.ispartofJournal of Cancer Research and Clinical Oncologyen_HK
dc.subjectConcurrent methylationen_HK
dc.subjectMethylation profileen_HK
dc.subjectOvarian tumorsen_HK
dc.subjectTumor suppressor genesen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenes, Tumor Suppressoren_HK
dc.subject.meshHumansen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshNeoplasm Recurrence, Localen_HK
dc.subject.meshOvarian Neoplasms - genetics - metabolismen_HK
dc.subject.meshOvary - metabolismen_HK
dc.subject.meshSurvival Analysisen_HK
dc.titleMethylation profile in benign, borderline and malignant ovarian tumorsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0171-5216&volume=133&issue=5&spage=331&epage=341&date=2007&atitle=Methylation+profile+in+benign,+borderline+and+malignant+ovarian+tumors+en_HK
dc.identifier.emailLiu, VWS: vwsliu@hkusua.hku.hken_HK
dc.identifier.emailLiu, SS: stephasl@hku.hken_HK
dc.identifier.emailCheung, ANY: anycheun@hkucc.hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.authorityLiu, VWS=rp00341en_HK
dc.identifier.authorityLiu, SS=rp00372en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s00432-006-0178-5en_HK
dc.identifier.pmid17177027-
dc.identifier.scopuseid_2-s2.0-34248192360en_HK
dc.identifier.hkuros130484en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34248192360&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume133en_HK
dc.identifier.issue5en_HK
dc.identifier.spage331en_HK
dc.identifier.epage341en_HK
dc.identifier.isiWOS:000245294700007-
dc.publisher.placeGermanyen_HK
dc.identifier.scopusauthoridTam, KF=35622901400en_HK
dc.identifier.scopusauthoridLiu, VWS=7006405113en_HK
dc.identifier.scopusauthoridLiu, SS=37102450400en_HK
dc.identifier.scopusauthoridTsang, PCK=7102404070en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK
dc.identifier.scopusauthoridYip, AMW=19838748300en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK

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