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- PMID: 12661010
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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
Title | 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 |
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Authors | |
Issue Date | 2003 |
Publisher | John 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? |
Abstract | It 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 Identifier | http://hdl.handle.net/10722/67727 |
ISSN | 2021 Impact Factor: 4.263 2020 SCImago Journal Rankings: 1.754 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Deng, W | en_HK |
dc.contributor.author | Tsao, SW | en_HK |
dc.contributor.author | Guan, XY | en_HK |
dc.contributor.author | Lucas, JN | en_HK |
dc.contributor.author | Cheung, ALM | en_HK |
dc.date.accessioned | 2010-09-06T05:57:43Z | - |
dc.date.available | 2010-09-06T05:57:43Z | - |
dc.date.issued | 2003 | en_HK |
dc.identifier.citation | Genes Chromosomes And Cancer, 2003, v. 37 n. 1, p. 92-97 | en_HK |
dc.identifier.issn | 1045-2257 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/67727 | - |
dc.description.abstract | It 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.language | eng | en_HK |
dc.publisher | John Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/38250 | en_HK |
dc.relation.ispartof | Genes Chromosomes and Cancer | en_HK |
dc.rights | Genes, Chromosomes & Cancer. Copyright © John Wiley & Sons, Inc. | en_HK |
dc.subject.mesh | Cell Line | en_HK |
dc.subject.mesh | Chromosome Aberrations | en_HK |
dc.subject.mesh | Chromosome Painting - methods - statistics & numerical data | en_HK |
dc.subject.mesh | Chromosomes, Human - genetics - physiology | en_HK |
dc.subject.mesh | Epithelial Cells - chemistry - metabolism - pathology | en_HK |
dc.subject.mesh | Female | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | In Situ Hybridization, Fluorescence - methods - statistics & numerical data | en_HK |
dc.subject.mesh | Ovary - pathology | en_HK |
dc.subject.mesh | Telomere - genetics - metabolism - physiology | en_HK |
dc.title | 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 | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+study | en_HK |
dc.identifier.email | Deng, W: wdeng@hkucc.hku.hk | en_HK |
dc.identifier.email | Tsao, SW: gswtsao@hku.hk | en_HK |
dc.identifier.email | Guan, XY: xyguan@hkucc.hku.hk | en_HK |
dc.identifier.email | Cheung, ALM: lmcheung@hku.hk | en_HK |
dc.identifier.authority | Deng, W=rp01640 | en_HK |
dc.identifier.authority | Tsao, SW=rp00399 | en_HK |
dc.identifier.authority | Guan, XY=rp00454 | en_HK |
dc.identifier.authority | Cheung, ALM=rp00332 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1002/gcc.10190 | en_HK |
dc.identifier.pmid | 12661010 | en_HK |
dc.identifier.scopus | eid_2-s2.0-0037402984 | en_HK |
dc.identifier.hkuros | 76478 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0037402984&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 37 | en_HK |
dc.identifier.issue | 1 | en_HK |
dc.identifier.spage | 92 | en_HK |
dc.identifier.epage | 97 | en_HK |
dc.identifier.isi | WOS:000182096400010 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Deng, W=7202223673 | en_HK |
dc.identifier.scopusauthorid | Tsao, SW=7102813116 | en_HK |
dc.identifier.scopusauthorid | Guan, XY=7201463221 | en_HK |
dc.identifier.scopusauthorid | Lucas, JN=7402441937 | en_HK |
dc.identifier.scopusauthorid | Cheung, ALM=7401806497 | en_HK |
dc.identifier.issnl | 1045-2257 | - |