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Article: Immortalization of human extravillous cytotrophoblasts by human papilloma virus gene E6E7: Sequential cytogenetic and molecular genetic characterization

TitleImmortalization of human extravillous cytotrophoblasts by human papilloma virus gene E6E7: Sequential cytogenetic and molecular genetic characterization
Authors
Issue Date2005
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene
Citation
Cancer Genetics And Cytogenetics, 2005, v. 163 n. 1, p. 30-37 How to Cite?
AbstractExtravillous cytotrophoblast (EVCT) cultures from the normal placentas of three pregnant women were transfected by HPVE6E7. Sequential cytogenetic and molecular analyses were performed to delineate genetic events that may be critical for cell immortalization. One line, PE1-E6E7, was immortalized successfully, whereas 2 other lines, PE3-E6E7 and PE4-E6E7, could not be maintained beyond crisis. Before crisis, the majority of cells in all lines were karyotypically normal. During the early stages of crisis, there was progressive telomere shortening. Most cells were karyotypically abnormal, with extreme cytogenetic divergence and a predominance of telomeric association and dicentric chromosomes affecting many chromosomes. At the later stages of crisis, the karyotype became more convergent with a drastic decrease in nonclonal aberrations. In PE1-E6E7, after crisis the karyotype was complex, with frequent centromeric rearrangements in the form of isochromosomes and whole-arm translocations. There were unbalanced structural aberrations and numerical changes, including loss of chromosome 13, that could be traced throughout the evolution of the line. These findings support the concept that immortalization is a relatively rare and nonrandom event that occurs only in cells that have acquired the necessary or critical genetic alterations. Telomeric dysfunction may be an important mechanism leading to the acquisition of complex karyotypical aberrations. © 2005 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67569
ISSN
2012 Impact Factor: 1.929
2013 SCImago Journal Rankings: 0.872
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorJin, Yen_HK
dc.contributor.authorFeng, HCen_HK
dc.contributor.authorDeng, Wen_HK
dc.contributor.authorZhang, Hen_HK
dc.contributor.authorLv, Men_HK
dc.contributor.authorJin, Cen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2010-09-06T05:56:18Z-
dc.date.available2010-09-06T05:56:18Z-
dc.date.issued2005en_HK
dc.identifier.citationCancer Genetics And Cytogenetics, 2005, v. 163 n. 1, p. 30-37en_HK
dc.identifier.issn0165-4608en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67569-
dc.description.abstractExtravillous cytotrophoblast (EVCT) cultures from the normal placentas of three pregnant women were transfected by HPVE6E7. Sequential cytogenetic and molecular analyses were performed to delineate genetic events that may be critical for cell immortalization. One line, PE1-E6E7, was immortalized successfully, whereas 2 other lines, PE3-E6E7 and PE4-E6E7, could not be maintained beyond crisis. Before crisis, the majority of cells in all lines were karyotypically normal. During the early stages of crisis, there was progressive telomere shortening. Most cells were karyotypically abnormal, with extreme cytogenetic divergence and a predominance of telomeric association and dicentric chromosomes affecting many chromosomes. At the later stages of crisis, the karyotype became more convergent with a drastic decrease in nonclonal aberrations. In PE1-E6E7, after crisis the karyotype was complex, with frequent centromeric rearrangements in the form of isochromosomes and whole-arm translocations. There were unbalanced structural aberrations and numerical changes, including loss of chromosome 13, that could be traced throughout the evolution of the line. These findings support the concept that immortalization is a relatively rare and nonrandom event that occurs only in cells that have acquired the necessary or critical genetic alterations. Telomeric dysfunction may be an important mechanism leading to the acquisition of complex karyotypical aberrations. © 2005 Elsevier 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.meshCells, Cultureden_HK
dc.subject.meshChorionic Villi - ultrastructure - virologyen_HK
dc.subject.meshChromosome Aberrationsen_HK
dc.subject.meshChromosome Bandingen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenes, Viralen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIn Situ Hybridization, Fluorescenceen_HK
dc.subject.meshKaryotypingen_HK
dc.subject.meshPapillomaviridae - geneticsen_HK
dc.subject.meshPlacenta - cytology - virologyen_HK
dc.subject.meshPregnancyen_HK
dc.subject.meshTelomere - geneticsen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshTranslocation, Geneticen_HK
dc.titleImmortalization of human extravillous cytotrophoblasts by human papilloma virus gene E6E7: Sequential cytogenetic and molecular genetic characterizationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0165-4608&volume=163&spage=30&epage=37&date=2005&atitle=Immortalization+of+human+extravillous+cytotrophoblasts+by+human+papilloma+virus+gene+E6E7:+sequential+cytogenetic+and+molecular+genetic+characterizationen_HK
dc.identifier.emailDeng, W: wdeng@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hku.hken_HK
dc.identifier.emailKwong, YL: ylkwong@hku.hken_HK
dc.identifier.authorityDeng, W=rp01640en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.cancergencyto.2005.04.020en_HK
dc.identifier.pmid16271953-
dc.identifier.scopuseid_2-s2.0-27744608383en_HK
dc.identifier.hkuros113134en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-27744608383&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume163en_HK
dc.identifier.issue1en_HK
dc.identifier.spage30en_HK
dc.identifier.epage37en_HK
dc.identifier.isiWOS:000233680800006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridJin, Y=7404457413en_HK
dc.identifier.scopusauthoridFeng, HC=7401736336en_HK
dc.identifier.scopusauthoridDeng, W=7202223673en_HK
dc.identifier.scopusauthoridZhang, H=8965962000en_HK
dc.identifier.scopusauthoridLv, M=55222421600en_HK
dc.identifier.scopusauthoridJin, C=7401659093en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK

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