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Article: The increase of mitochondrial DNA content in endometrial adenocarcinoma cells: A quantitative study using laser-captured microdissected tissues

TitleThe increase of mitochondrial DNA content in endometrial adenocarcinoma cells: A quantitative study using laser-captured microdissected tissues
Authors
KeywordsCopy number
Endometrial carcinoma
Laser capture microdissection
Microsatellite instability
Mitochondrial DNA
Issue Date2005
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ygyno
Citation
Gynecologic Oncology, 2005, v. 98 n. 1, p. 104-110 How to Cite?
AbstractObjective. Microsatellite instability (MSI) is a frequent genetic event in the D-loop region (which controls mitochondrial DNA (mtDNA) replication) of mitochondrial genome of endometrial cancer. We therefore investigated the relationship between mtMSI and mtDNA content in endometrial cancer. Methods. Tumor tissues from 65 cancer patients and normal tissues from 41 non-cancer patients were used in this study. Pure endometrial adenocarcinoma cells and normal endometrial glandular epithelial cells were collected by laser capture microdissection, and analyzed for levels of mtDNA copy number by real-time quantitative PCR. Results. Our data show that mtDNA copy number was not related with age in both endometrial cancer and normal endometrium cells. Great inter-individual variations in mtDNA copy number in endometrial cancer group were found; and mtDNA content was significantly larger than that in normal endometrium group. About 2-fold increase of mtDNA copy number was found in endometrial adenocarcinoma compared with normal endometrial glandular epithelium (P = 0.001). In particular, the analysis also shows that the copy number of mtDNA in the cases that carried the mtMSI at nucleotide position 303 was significantly higher than that of the negative cases (P = 0.048). Conclusions. Our data indicate that mtDNA copy number increased during endometrial cancer development. There is also a correlation between the mtDNA instability and mtDNA content in endometrial cancer cells. Role of mitochondrial genome changes in carcinogenesis warrants further investigation. © 2005 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/87490
ISSN
2015 Impact Factor: 4.198
2015 SCImago Journal Rankings: 2.284
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_HK
dc.contributor.authorLiu, VWSen_HK
dc.contributor.authorXue, WCen_HK
dc.contributor.authorTsang, PCKen_HK
dc.contributor.authorCheung, ANYen_HK
dc.contributor.authorNgan, HYSen_HK
dc.date.accessioned2010-09-06T09:30:20Z-
dc.date.available2010-09-06T09:30:20Z-
dc.date.issued2005en_HK
dc.identifier.citationGynecologic Oncology, 2005, v. 98 n. 1, p. 104-110en_HK
dc.identifier.issn0090-8258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/87490-
dc.description.abstractObjective. Microsatellite instability (MSI) is a frequent genetic event in the D-loop region (which controls mitochondrial DNA (mtDNA) replication) of mitochondrial genome of endometrial cancer. We therefore investigated the relationship between mtMSI and mtDNA content in endometrial cancer. Methods. Tumor tissues from 65 cancer patients and normal tissues from 41 non-cancer patients were used in this study. Pure endometrial adenocarcinoma cells and normal endometrial glandular epithelial cells were collected by laser capture microdissection, and analyzed for levels of mtDNA copy number by real-time quantitative PCR. Results. Our data show that mtDNA copy number was not related with age in both endometrial cancer and normal endometrium cells. Great inter-individual variations in mtDNA copy number in endometrial cancer group were found; and mtDNA content was significantly larger than that in normal endometrium group. About 2-fold increase of mtDNA copy number was found in endometrial adenocarcinoma compared with normal endometrial glandular epithelium (P = 0.001). In particular, the analysis also shows that the copy number of mtDNA in the cases that carried the mtMSI at nucleotide position 303 was significantly higher than that of the negative cases (P = 0.048). Conclusions. Our data indicate that mtDNA copy number increased during endometrial cancer development. There is also a correlation between the mtDNA instability and mtDNA content in endometrial cancer cells. Role of mitochondrial genome changes in carcinogenesis warrants further investigation. © 2005 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ygynoen_HK
dc.relation.ispartofGynecologic Oncologyen_HK
dc.subjectCopy numberen_HK
dc.subjectEndometrial carcinomaen_HK
dc.subjectLaser capture microdissectionen_HK
dc.subjectMicrosatellite instabilityen_HK
dc.subjectMitochondrial DNAen_HK
dc.subject.meshAdenocarcinoma - geneticsen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAge Factorsen_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshDNA, Mitochondrial - genetics - isolation & purification - metabolismen_HK
dc.subject.meshEndometrial Neoplasms - geneticsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGlobins - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIndividualityen_HK
dc.subject.meshMicrodissectionen_HK
dc.subject.meshMicrosatellite Repeats - geneticsen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.titleThe increase of mitochondrial DNA content in endometrial adenocarcinoma cells: A quantitative study using laser-captured microdissected tissuesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0090-8258&volume=98&spage=104&epage=110&date=2005&atitle=The+Increase+Of+Mitochondrial+Dna+Content+In+Endometrial+Adenocarcinoma+Cells:+A+Quantitative+Study+Using+Laser-captured+Microdissected+Tissuesen_HK
dc.identifier.emailLiu, VWS: vwsliu@hkusua.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.authorityCheung, ANY=rp00542en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.ygyno.2005.04.015en_HK
dc.identifier.pmid15921730-
dc.identifier.scopuseid_2-s2.0-20444455342en_HK
dc.identifier.hkuros113328en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-20444455342&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume98en_HK
dc.identifier.issue1en_HK
dc.identifier.spage104en_HK
dc.identifier.epage110en_HK
dc.identifier.isiWOS:000230284200017-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWang, Y=8637619000en_HK
dc.identifier.scopusauthoridLiu, VWS=7006405113en_HK
dc.identifier.scopusauthoridXue, WC=7103165268en_HK
dc.identifier.scopusauthoridTsang, PCK=7102404070en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK

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