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Article: Telomere-mediated mitotic disturbances in immortalized ovarian epithelial cells reproduce chromosomal and breakpoints from ovarian carcinoma

TitleTelomere-mediated mitotic disturbances in immortalized ovarian epithelial cells reproduce chromosomal and breakpoints from ovarian carcinoma
Authors
Issue Date2005
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/38250
Citation
Genes Chromosomes And Cancer, 2005, v. 42 n. 1, p. 22-33 How to Cite?
AbstractOvarian carcinomas (OCs) often exhibit highly complex cytogenetic changes. Abnormal chromosome segregation at mitosis is one potential mechanism for genomic rearrangements in tumors. In this study, OCs were demonstrated to have dysfunctional short telomeres, anaphase bridging, and multipolar mitoses with supernumerary centrosomes. When normal human ovarian surface epithelial (HOSE) cells were transfected with human papilloma virus 16 e6/e7 genes and subsequently driven into telomere crisis, the same set of mitotic disturbances occurred in a distinct sequence, initiated by telomere dysfunction, followed by anaphase bridging, and then supernumerary centrosomes and multipolar mitoses. The anaphase bridges resolved either by kinetochore-spindle detachment, corresponding to whole-chromosome losses in the HOSE karyotypes, or by extensive fragmentation of intercentromeric DNA sequences, corresponding to a high frequency of pericentromeric rearrangements. At later passages, the high degree of instability at telomere crisis was moderated by telomerase expression and centrosome coalescence, ultimately leading to a level of mitotic instability that was highly similar to that in OC cell lines and to complex karyotypes that were similar to those observed in high-grade OCs. This suggests that a significant proportion of the structural chromosome changes and genomic losses in OC are caused by a specific sequence of mitotic disturbances triggered by telomere crisis. That the model did not produce any of the whole-chromosome gains observed in OC indicates that these changes develop through a different mechanism. © 2004 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/149792
ISSN
2015 Impact Factor: 3.96
2015 SCImago Journal Rankings: 2.210
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGisselsson, Den_US
dc.contributor.authorLv, Men_US
dc.contributor.authorTsao, SWen_US
dc.contributor.authorMan, Cen_US
dc.contributor.authorJin, Cen_US
dc.contributor.authorHöglund, Men_US
dc.contributor.authorYok, LKen_US
dc.contributor.authorJin, Yen_US
dc.date.accessioned2012-06-26T05:58:46Z-
dc.date.available2012-06-26T05:58:46Z-
dc.date.issued2005en_US
dc.identifier.citationGenes Chromosomes And Cancer, 2005, v. 42 n. 1, p. 22-33en_US
dc.identifier.issn1045-2257en_US
dc.identifier.urihttp://hdl.handle.net/10722/149792-
dc.description.abstractOvarian carcinomas (OCs) often exhibit highly complex cytogenetic changes. Abnormal chromosome segregation at mitosis is one potential mechanism for genomic rearrangements in tumors. In this study, OCs were demonstrated to have dysfunctional short telomeres, anaphase bridging, and multipolar mitoses with supernumerary centrosomes. When normal human ovarian surface epithelial (HOSE) cells were transfected with human papilloma virus 16 e6/e7 genes and subsequently driven into telomere crisis, the same set of mitotic disturbances occurred in a distinct sequence, initiated by telomere dysfunction, followed by anaphase bridging, and then supernumerary centrosomes and multipolar mitoses. The anaphase bridges resolved either by kinetochore-spindle detachment, corresponding to whole-chromosome losses in the HOSE karyotypes, or by extensive fragmentation of intercentromeric DNA sequences, corresponding to a high frequency of pericentromeric rearrangements. At later passages, the high degree of instability at telomere crisis was moderated by telomerase expression and centrosome coalescence, ultimately leading to a level of mitotic instability that was highly similar to that in OC cell lines and to complex karyotypes that were similar to those observed in high-grade OCs. This suggests that a significant proportion of the structural chromosome changes and genomic losses in OC are caused by a specific sequence of mitotic disturbances triggered by telomere crisis. That the model did not produce any of the whole-chromosome gains observed in OC indicates that these changes develop through a different mechanism. © 2004 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/38250en_US
dc.relation.ispartofGenes Chromosomes and Canceren_US
dc.subject.meshCell Cycle - Genetics - Physiologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshChromosome Aberrationsen_US
dc.subject.meshChromosome Deletionen_US
dc.subject.meshChromosomes, Human - Geneticsen_US
dc.subject.meshEpithelial Cells - Cytologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expression Profilingen_US
dc.subject.meshHumansen_US
dc.subject.meshKaryotypingen_US
dc.subject.meshMitosis - Physiologyen_US
dc.subject.meshOvarian Neoplasms - Genetics - Pathologyen_US
dc.subject.meshTelomere - Genetics - Ultrastructureen_US
dc.titleTelomere-mediated mitotic disturbances in immortalized ovarian epithelial cells reproduce chromosomal and breakpoints from ovarian carcinomaen_US
dc.typeArticleen_US
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_US
dc.identifier.authorityTsao, SW=rp00399en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/gcc.20094en_US
dc.identifier.pmid15390185-
dc.identifier.scopuseid_2-s2.0-9644272618en_US
dc.identifier.hkuros99340-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-9644272618&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume42en_US
dc.identifier.issue1en_US
dc.identifier.spage22en_US
dc.identifier.epage33en_US
dc.identifier.isiWOS:000225367900003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridGisselsson, D=7003453988en_US
dc.identifier.scopusauthoridLv, M=55222421600en_US
dc.identifier.scopusauthoridTsao, SW=7102813116en_US
dc.identifier.scopusauthoridMan, C=7005722377en_US
dc.identifier.scopusauthoridJin, C=7401659093en_US
dc.identifier.scopusauthoridHöglund, M=7006658976en_US
dc.identifier.scopusauthoridYok, LK=6508259849en_US
dc.identifier.scopusauthoridJin, Y=7404457413en_US

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