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Article: Role of short telomeres in inducing preferential chromosomal aberrations in human ovarian surface epithelial cells: A combined telomere quantitative fluorescence in situ hybridization and whole-chromosome painting study

TitleRole of short telomeres in inducing preferential chromosomal aberrations in human ovarian surface epithelial cells: A combined telomere quantitative fluorescence in situ hybridization and whole-chromosome painting study
Authors
Issue Date2003
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, 2003, v. 37 n. 1, p. 92-97 How to Cite?
AbstractIt is well established that specific cancers and immortalized cells have nonrandom chromosome aberrations. However, little is understood about the underlying mechanism that initiates these aberrations in human cells. To examine whether human chromosomes with the shortest telomeres initiate the preferential chromosomal aberrations before cellular immortalization, we simultaneously applied telomere quantitative fluorescence in situ hybridization and specific whole-chromosome painting on chromosomes 1, 5, 8, 17, 19, and 20 in human ovarian surface epithelial (HOSE 6-3) cells expressing human papilloma viral oncogenes (HPV 16 E6E7). The HIPV 16 E6E7-expressing cells, with extended in vitro life span and telomerase-negative status, were previously identified as having nonrandom chromosomal imbalances and high frequencies of dicentrics. Our analyses showed that among six pairs of targeted chromosomes, chromosomes 8 and 20 showed critically short telomeres with an undetectable telomere signal in more than 50% of cells analyzed. These chromosomes with the critically short telomeres were preferentially involved in various types of chromosomal aberrations including dicentrics, translocations, breaks, insertions, and losses or gains of chromosomal elements. Our findings suggest that nonrandom chromosome aberrations in HOSE cells occurring before cellular immortalization could be caused by the telomere length heterogeneity. © 2003 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/67727
ISSN
2015 Impact Factor: 3.96
2015 SCImago Journal Rankings: 2.210
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDeng, Wen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorGuan, XYen_HK
dc.contributor.authorLucas, JNen_HK
dc.contributor.authorCheung, ALMen_HK
dc.date.accessioned2010-09-06T05:57:43Z-
dc.date.available2010-09-06T05:57:43Z-
dc.date.issued2003en_HK
dc.identifier.citationGenes Chromosomes And Cancer, 2003, v. 37 n. 1, p. 92-97en_HK
dc.identifier.issn1045-2257en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67727-
dc.description.abstractIt is well established that specific cancers and immortalized cells have nonrandom chromosome aberrations. However, little is understood about the underlying mechanism that initiates these aberrations in human cells. To examine whether human chromosomes with the shortest telomeres initiate the preferential chromosomal aberrations before cellular immortalization, we simultaneously applied telomere quantitative fluorescence in situ hybridization and specific whole-chromosome painting on chromosomes 1, 5, 8, 17, 19, and 20 in human ovarian surface epithelial (HOSE 6-3) cells expressing human papilloma viral oncogenes (HPV 16 E6E7). The HIPV 16 E6E7-expressing cells, with extended in vitro life span and telomerase-negative status, were previously identified as having nonrandom chromosomal imbalances and high frequencies of dicentrics. Our analyses showed that among six pairs of targeted chromosomes, chromosomes 8 and 20 showed critically short telomeres with an undetectable telomere signal in more than 50% of cells analyzed. These chromosomes with the critically short telomeres were preferentially involved in various types of chromosomal aberrations including dicentrics, translocations, breaks, insertions, and losses or gains of chromosomal elements. Our findings suggest that nonrandom chromosome aberrations in HOSE cells occurring before cellular immortalization could be caused by the telomere length heterogeneity. © 2003 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/38250en_HK
dc.relation.ispartofGenes Chromosomes and Canceren_HK
dc.rightsGenes, Chromosomes & Cancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshCell Lineen_HK
dc.subject.meshChromosome Aberrationsen_HK
dc.subject.meshChromosome Painting - methods - statistics & numerical dataen_HK
dc.subject.meshChromosomes, Human - genetics - physiologyen_HK
dc.subject.meshEpithelial Cells - chemistry - metabolism - pathologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIn Situ Hybridization, Fluorescence - methods - statistics & numerical dataen_HK
dc.subject.meshOvary - pathologyen_HK
dc.subject.meshTelomere - genetics - metabolism - physiologyen_HK
dc.titleRole of short telomeres in inducing preferential chromosomal aberrations in human ovarian surface epithelial cells: A combined telomere quantitative fluorescence in situ hybridization and whole-chromosome painting studyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1045-2257&volume=37&spage=92&epage=97&date=2003&atitle=Role+of+short+telomeres+in+inducing+preferential+chromosomal+aberrations+in+human+ovarian+surface+epithelial+cells:+a+combined+telomere+quantitative+fluorescence+in+situ+hybridization+and+whole-chromosome+painting+studyen_HK
dc.identifier.emailDeng, W: wdeng@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hku.hken_HK
dc.identifier.emailGuan, XY: xyguan@hkucc.hku.hken_HK
dc.identifier.emailCheung, ALM: lmcheung@hku.hken_HK
dc.identifier.authorityDeng, W=rp01640en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/gcc.10190en_HK
dc.identifier.pmid12661010en_HK
dc.identifier.scopuseid_2-s2.0-0037402984en_HK
dc.identifier.hkuros76478en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037402984&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume37en_HK
dc.identifier.issue1en_HK
dc.identifier.spage92en_HK
dc.identifier.epage97en_HK
dc.identifier.isiWOS:000182096400010-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridDeng, W=7202223673en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.scopusauthoridLucas, JN=7402441937en_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK

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