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Article: Nonrandom chromosomal imbalances in human ovarian surface epithelial cells immortalized by HPV16-E6E7 viral oncogenes

TitleNonrandom chromosomal imbalances in human ovarian surface epithelial cells immortalized by HPV16-E6E7 viral oncogenes
Authors
Issue Date2001
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene
Citation
Cancer Genetics And Cytogenetics, 2001, v. 130 n. 2, p. 141-149 How to Cite?
AbstractWe had previously immortalized human ovarian surface epithelial (HOSE) cells using HPV16E6E7 ORFs. In order to identify crucial genetic events involved during cell immortalization, the genomic profile of immortalization of five HOSE cell lines was analyzed by comparative genomic hybridization. Our results showed that chromosomal imbalance was common in HOSE cells after immortalization. The common chromosomal imbalances identified in immortal HOSE cells are: +19q13.1 (5/5 lines), -13q12∼qter (4/5 lines), +5q15∼q33 (3/5 lines), +20q11.2∼q13.2 (3/5 lines) and -22q11.2∼qter (3/5 lines). Other chromosomal imbalances, which were detected in two of the five immortal HOSE cell lines, included gains on chromosome 1 and 11q12∼q13, and losses on 2p, 4q, 8p, 10p and 11q14∼qter. The chromosomal imbalances observed in HOSE cells before immortalization include -8pter∼p11.2, -11q23∼qter, -13q12∼qter and +19 which may represent early genetic events during cell immortalization. The genomic profile was examined in one HOSE cell line (HOSE 6-3) at various stages of immortalization. The genomic profiles of HOSE 6-3 cells after crisis were largely stable. A few additional chromosomal imbalances were detected in the immortalized HOSE cells after an extensive culture period including +11pter∼q23, -15q23∼qter, and +17q12∼qter. Identification of nonrandom chromosomal imbalance in immortalized HOSE cells may facilitate the identification of specific chromosomes harboring genes involved in the immortalization of human ovarian surface epithelial cells. © 2001 Elsevier Science Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67801
ISSN
2012 Impact Factor: 1.929
2013 SCImago Journal Rankings: 0.872
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorWong, Nen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorWan, TSKen_HK
dc.contributor.authorFung, LFen_HK
dc.contributor.authorLancaster, WDen_HK
dc.contributor.authorGregoire, Len_HK
dc.contributor.authorWong, YCen_HK
dc.date.accessioned2010-09-06T05:58:22Z-
dc.date.available2010-09-06T05:58:22Z-
dc.date.issued2001en_HK
dc.identifier.citationCancer Genetics And Cytogenetics, 2001, v. 130 n. 2, p. 141-149en_HK
dc.identifier.issn0165-4608en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67801-
dc.description.abstractWe had previously immortalized human ovarian surface epithelial (HOSE) cells using HPV16E6E7 ORFs. In order to identify crucial genetic events involved during cell immortalization, the genomic profile of immortalization of five HOSE cell lines was analyzed by comparative genomic hybridization. Our results showed that chromosomal imbalance was common in HOSE cells after immortalization. The common chromosomal imbalances identified in immortal HOSE cells are: +19q13.1 (5/5 lines), -13q12∼qter (4/5 lines), +5q15∼q33 (3/5 lines), +20q11.2∼q13.2 (3/5 lines) and -22q11.2∼qter (3/5 lines). Other chromosomal imbalances, which were detected in two of the five immortal HOSE cell lines, included gains on chromosome 1 and 11q12∼q13, and losses on 2p, 4q, 8p, 10p and 11q14∼qter. The chromosomal imbalances observed in HOSE cells before immortalization include -8pter∼p11.2, -11q23∼qter, -13q12∼qter and +19 which may represent early genetic events during cell immortalization. The genomic profile was examined in one HOSE cell line (HOSE 6-3) at various stages of immortalization. The genomic profiles of HOSE 6-3 cells after crisis were largely stable. A few additional chromosomal imbalances were detected in the immortalized HOSE cells after an extensive culture period including +11pter∼q23, -15q23∼qter, and +17q12∼qter. Identification of nonrandom chromosomal imbalance in immortalized HOSE cells may facilitate the identification of specific chromosomes harboring genes involved in the immortalization of human ovarian surface epithelial cells. © 2001 Elsevier Science Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergeneen_HK
dc.relation.ispartofCancer Genetics and Cytogeneticsen_HK
dc.rightsCancer Genetics and Cytogenetics. Copyright © Elsevier Inc.en_HK
dc.subject.meshCell Lineen_HK
dc.subject.meshCell Transformation, Viralen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshChromosome Aberrationsen_HK
dc.subject.meshChromosomes, Human, Pair 13en_HK
dc.subject.meshChromosomes, Human, Pair 19en_HK
dc.subject.meshChromosomes, Human, Pair 20en_HK
dc.subject.meshChromosomes, Human, Pair 22en_HK
dc.subject.meshChromosomes, Human, Pair 5en_HK
dc.subject.meshEpithelial Cells - pathologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenetic Techniquesen_HK
dc.subject.meshHumansen_HK
dc.subject.meshNucleic Acid Hybridizationen_HK
dc.subject.meshOncogene Proteins, Viral - geneticsen_HK
dc.subject.meshOpen Reading Framesen_HK
dc.subject.meshOvarian Neoplasms - geneticsen_HK
dc.subject.meshOvary - pathologyen_HK
dc.subject.meshPapillomavirus E7 Proteinsen_HK
dc.subject.meshRepressor Proteinsen_HK
dc.titleNonrandom chromosomal imbalances in human ovarian surface epithelial cells immortalized by HPV16-E6E7 viral oncogenesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0165-4608&volume=130&spage=141&epage=149&date=2001&atitle=Nonrandom+chromosomal+imbalances+in+human+ovarian+surface+epithelial+cells+immortalized+by+HPV16-E6E7+viral+oncogenesen_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0165-4608(01)00473-3en_HK
dc.identifier.pmid11675135-
dc.identifier.scopuseid_2-s2.0-0035886616en_HK
dc.identifier.hkuros64350en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035886616&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume130en_HK
dc.identifier.issue2en_HK
dc.identifier.spage141en_HK
dc.identifier.epage149en_HK
dc.identifier.isiWOS:000171934100007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridWong, N=7202836653en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridLiu, Y=26643293600en_HK
dc.identifier.scopusauthoridWan, TSK=25623981600en_HK
dc.identifier.scopusauthoridFung, LF=35910298200en_HK
dc.identifier.scopusauthoridLancaster, WD=7006256157en_HK
dc.identifier.scopusauthoridGregoire, L=7006932577en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK

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