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Conference Paper: Telomere erosion and numerical chromosomal instability in human cells undergoing immortalization

TitleTelomere erosion and numerical chromosomal instability in human cells undergoing immortalization
Authors
Issue Date2006
PublisherFederation of American Societies for Experimental Biology.
Citation
The F A S E B Journal, 2006, v. 20 n. 5, p. A894 Abstract no. 587.1 How to Cite?
AbstractIt has been a long-standing mystery why pre-immortal, immortalized and cancer cells universally have nonrandom numerical chromosome abnormalities. The objective of this study was to test whether telomere erosion induces numerical chromosome instability. Five human epithelial cells expressing human papillomavirus oncogenes, HPV16-E6 and E7, were used as cell models. Metaphase cells were collected for analyses of telomere profiles on individual chromosomes and numerical chromosome abnormalities in the entire process of immortalization. Quantitation of individual telomere signals were performed using combined quantitative telomere fluorescence in situ hybridization (Q-FISH) and Spectral Karyotyping (SKY). Our results showed persistent numerical chromosome instability, manifested as dynamic gains or losses of whole-chromosomes, in all the cell lines from pre-immortal stage to crisis. There was a general trend of dynamic increases in the frequencies of near-diploid (chromosome number = 40–47) or hypo-tetraploid (chromosome number = 81–91) cells, but near triploid and hyper-tetraploid cells were infrequently generated. However, there was no consistent relationship between the existence of the shortest telomeres and the frequencies of numerical abnormalities on individual chromosomes in the whole-genome of each analyzed cell line. Our data, therefore, indicate that telomere dysfunction does not seem to play a significant role in numerical chromosome instability in human cells undergoing immortalization. [This study was supported by a grant from the Research Grants Council of the Hong Kong Special Administrative Region, China, Project No. HKU 7385/03M, and a HKU Small Project Grant (2005-06)]
Persistent Identifierhttp://hdl.handle.net/10722/95579
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorCheung, Aen_HK
dc.contributor.authorDeng, Wen_HK
dc.contributor.authorTsao, GSWen_HK
dc.contributor.authorGuan, XYen_HK
dc.date.accessioned2010-09-25T16:06:42Z-
dc.date.available2010-09-25T16:06:42Z-
dc.date.issued2006en_HK
dc.identifier.citationThe F A S E B Journal, 2006, v. 20 n. 5, p. A894 Abstract no. 587.1en_HK
dc.identifier.issn0892-6638en_HK
dc.identifier.urihttp://hdl.handle.net/10722/95579-
dc.description.abstractIt has been a long-standing mystery why pre-immortal, immortalized and cancer cells universally have nonrandom numerical chromosome abnormalities. The objective of this study was to test whether telomere erosion induces numerical chromosome instability. Five human epithelial cells expressing human papillomavirus oncogenes, HPV16-E6 and E7, were used as cell models. Metaphase cells were collected for analyses of telomere profiles on individual chromosomes and numerical chromosome abnormalities in the entire process of immortalization. Quantitation of individual telomere signals were performed using combined quantitative telomere fluorescence in situ hybridization (Q-FISH) and Spectral Karyotyping (SKY). Our results showed persistent numerical chromosome instability, manifested as dynamic gains or losses of whole-chromosomes, in all the cell lines from pre-immortal stage to crisis. There was a general trend of dynamic increases in the frequencies of near-diploid (chromosome number = 40–47) or hypo-tetraploid (chromosome number = 81–91) cells, but near triploid and hyper-tetraploid cells were infrequently generated. However, there was no consistent relationship between the existence of the shortest telomeres and the frequencies of numerical abnormalities on individual chromosomes in the whole-genome of each analyzed cell line. Our data, therefore, indicate that telomere dysfunction does not seem to play a significant role in numerical chromosome instability in human cells undergoing immortalization. [This study was supported by a grant from the Research Grants Council of the Hong Kong Special Administrative Region, China, Project No. HKU 7385/03M, and a HKU Small Project Grant (2005-06)]-
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology.en_HK
dc.relation.ispartofThe F A S E B Journalen_HK
dc.titleTelomere erosion and numerical chromosomal instability in human cells undergoing immortalizationen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0892-6638&volume=20 No. 5&spage=A894 No.587.1&epage=&date=2006&atitle=Chromosome/DNA:+aneuploidy+and+centromeres/kinetochores,+and+cohesion/chromosome+condensationen_HK
dc.identifier.emailCheung, A: lmcheung@hkucc.hku.hken_HK
dc.identifier.emailTsao, GSW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailGuan, XY: xyguan@hkucc.hku.hken_HK
dc.identifier.authorityCheung, A=rp00332en_HK
dc.identifier.authorityTsao, GSW=rp00399en_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.identifier.hkuros115239en_HK
dc.identifier.volume20en_HK
dc.identifier.spage894en_HK

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