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Article: Cytogenetic aberrations in immortalization of esophageal epithelial cells

TitleCytogenetic aberrations in immortalization of esophageal epithelial cells
Authors
Issue Date2006
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene
Citation
Cancer Genetics And Cytogenetics, 2006, v. 165 n. 1, p. 25-35 How to Cite?
AbstractTo define the early cytogenetic events important in esophageal carcinogenesis, we immortalized normal esophageal epithelial cells by overexpression of human papillomavirus type 16 E6/E7 (HPV16E6/E7) and human telomerase reverse transcriptase (hTERT), and characterized the chromosomal abnormalities serially before and after cellular immortalizaiton. During crisis, most cells had simple nonclonal karyotypic changes with cytogenetic divergence. Mitotically unstable chromosomes (i.e., telomere association and dicentric chromosomes) were the most common aberrations. After crisis, the karyotypic patterns were more convergent with nonrandom clonal changes. A few clones dominated the culture. Gain of chromosome 20q was consistently observed in four HPVE6/E7 immortalized esophageal lines, whereas amplification of chromosome 5q was preferentially found in hTERT immortalized cells. In addition, chromosomal aberrations of immortalized cells, including del(3p) and centromere rearrangements, were similar to those observed in esophageal cancer. Furthermore, in E6/E7-expressing cells, the frequency of negative telomere termini and anaphase bridges were high during crisis and low after crisis. These findings suggested that telomere dysfunction might be an important cause of cellular crisis, and the resultant chromosomal aberrations, mainly amplification of chromosome 20q or 5q, might be early genetic events required in esophageal cell immortalization. These alterations might be valuable models for further study of molecular mechanisms contributing to esophageal carcinogenesis. © 2006 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67944
ISSN
2012 Impact Factor: 1.929
2013 SCImago Journal Rankings: 0.872
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, Hen_HK
dc.contributor.authorJin, Yen_HK
dc.contributor.authorChen, Xen_HK
dc.contributor.authorJin, Cen_HK
dc.contributor.authorLaw, Sen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2010-09-06T05:59:41Z-
dc.date.available2010-09-06T05:59:41Z-
dc.date.issued2006en_HK
dc.identifier.citationCancer Genetics And Cytogenetics, 2006, v. 165 n. 1, p. 25-35en_HK
dc.identifier.issn0165-4608en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67944-
dc.description.abstractTo define the early cytogenetic events important in esophageal carcinogenesis, we immortalized normal esophageal epithelial cells by overexpression of human papillomavirus type 16 E6/E7 (HPV16E6/E7) and human telomerase reverse transcriptase (hTERT), and characterized the chromosomal abnormalities serially before and after cellular immortalizaiton. During crisis, most cells had simple nonclonal karyotypic changes with cytogenetic divergence. Mitotically unstable chromosomes (i.e., telomere association and dicentric chromosomes) were the most common aberrations. After crisis, the karyotypic patterns were more convergent with nonrandom clonal changes. A few clones dominated the culture. Gain of chromosome 20q was consistently observed in four HPVE6/E7 immortalized esophageal lines, whereas amplification of chromosome 5q was preferentially found in hTERT immortalized cells. In addition, chromosomal aberrations of immortalized cells, including del(3p) and centromere rearrangements, were similar to those observed in esophageal cancer. Furthermore, in E6/E7-expressing cells, the frequency of negative telomere termini and anaphase bridges were high during crisis and low after crisis. These findings suggested that telomere dysfunction might be an important cause of cellular crisis, and the resultant chromosomal aberrations, mainly amplification of chromosome 20q or 5q, might be early genetic events required in esophageal cell immortalization. These alterations might be valuable models for further study of molecular mechanisms contributing to esophageal carcinogenesis. © 2006 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.meshCell Line, Tumoren_HK
dc.subject.meshChromosome Aberrationsen_HK
dc.subject.meshDNA-Binding Proteins - geneticsen_HK
dc.subject.meshEsophageal Neoplasms - genetics - pathology - virologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIn Situ Hybridization, Fluorescenceen_HK
dc.subject.meshKaryotypingen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMucous Membrane - pathologyen_HK
dc.subject.meshPapillomaviridae - isolation & purificationen_HK
dc.subject.meshTelomerase - geneticsen_HK
dc.titleCytogenetic aberrations in immortalization of esophageal epithelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0165-4608&volume=165&issue=1&spage=25&epage=35&date=2006&atitle=Cytogenetic+aberrations+in+immortalization+of+esophageal+epithelial+cellsen_HK
dc.identifier.emailLaw, S: slaw@hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailKwong, YL: ylkwong@hku.hken_HK
dc.identifier.authorityLaw, S=rp00437en_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.2005.07.016en_HK
dc.identifier.pmid16490594-
dc.identifier.scopuseid_2-s2.0-32844475447en_HK
dc.identifier.hkuros117991en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-32844475447&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume165en_HK
dc.identifier.issue1en_HK
dc.identifier.spage25en_HK
dc.identifier.epage35en_HK
dc.identifier.isiWOS:000236133000004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZhang, H=8965962000en_HK
dc.identifier.scopusauthoridJin, Y=7404457413en_HK
dc.identifier.scopusauthoridChen, X=8252513600en_HK
dc.identifier.scopusauthoridJin, C=7401659093en_HK
dc.identifier.scopusauthoridLaw, S=7202241293en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK

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