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Article: Telomere dysfunction, genome instability and cancer

TitleTelomere dysfunction, genome instability and cancer
Authors
KeywordsCancer
Chromosomal instability
Genomic instability
Review
Telomere
Issue Date2008
PublisherFrontiers in Bioscience. The Journal's web site is located at http://www.frontbiosci.org/
Citation
Frontiers In Bioscience, 2008, v. 13 n. 6, p. 2075-2090 How to Cite?
AbstractTelomeres are highly specialized structures at the ends of chromosomes that are made up of tandem 5′-TTAGGG-3′ repeats and a number of telomere associated proteins. By forming loop structures, the very end of a telomere is concealed and distinguished from a DNA break, thus protecting chromosomes from end-to-end fusions, misrepair and degradation. Telomere length is maintained by an enzyme called telomerase which is very weak or undetectable in most normal human somatic cells. In telomerase-negative cells, telomeric DNA is progressively lost with cell divisions until the cells undergo replicative senescence, which serves as an intrinsic mechanism to prevent normal somatic cells from replicating indefinitely. In checkpoint defective cells, telomere dysfunction resulting from excessive telomere attrition or disruption of telomere structure may initiate chromosomal instability through end-to-end fusion of unprotected chromosomes. Through propagation of breakage-fusion-bridge (BFB) cycles, genetic aberrations characteristic of cancers, including aneuploidy, loss of heterozygosity, gene amplification and gene loss can be generated. In vitro, cells with extensive chromosomal instability succumb to crisis which is characterized by wide-spread cell death. It has been reported that cells surviving crisis either have activated telomerase, or use an alternative telomere lengthening (ALT) mechanism to stabilize the existing telomeres and alleviate chromosome instability. The immortalized post-crisis cells have the potential to acquire additional genetic alterations for malignant transformation. In this review, we summarize our knowledge on the association between telomere dysfunction, genomic instability and cancer development.
Persistent Identifierhttp://hdl.handle.net/10722/67886
ISSN
2015 Impact Factor: 2.484
2015 SCImago Journal Rankings: 1.583
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, ALMen_HK
dc.contributor.authorDeng, Wen_HK
dc.date.accessioned2010-09-06T05:59:10Z-
dc.date.available2010-09-06T05:59:10Z-
dc.date.issued2008en_HK
dc.identifier.citationFrontiers In Bioscience, 2008, v. 13 n. 6, p. 2075-2090en_HK
dc.identifier.issn1093-9946en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67886-
dc.description.abstractTelomeres are highly specialized structures at the ends of chromosomes that are made up of tandem 5′-TTAGGG-3′ repeats and a number of telomere associated proteins. By forming loop structures, the very end of a telomere is concealed and distinguished from a DNA break, thus protecting chromosomes from end-to-end fusions, misrepair and degradation. Telomere length is maintained by an enzyme called telomerase which is very weak or undetectable in most normal human somatic cells. In telomerase-negative cells, telomeric DNA is progressively lost with cell divisions until the cells undergo replicative senescence, which serves as an intrinsic mechanism to prevent normal somatic cells from replicating indefinitely. In checkpoint defective cells, telomere dysfunction resulting from excessive telomere attrition or disruption of telomere structure may initiate chromosomal instability through end-to-end fusion of unprotected chromosomes. Through propagation of breakage-fusion-bridge (BFB) cycles, genetic aberrations characteristic of cancers, including aneuploidy, loss of heterozygosity, gene amplification and gene loss can be generated. In vitro, cells with extensive chromosomal instability succumb to crisis which is characterized by wide-spread cell death. It has been reported that cells surviving crisis either have activated telomerase, or use an alternative telomere lengthening (ALT) mechanism to stabilize the existing telomeres and alleviate chromosome instability. The immortalized post-crisis cells have the potential to acquire additional genetic alterations for malignant transformation. In this review, we summarize our knowledge on the association between telomere dysfunction, genomic instability and cancer development.en_HK
dc.languageengen_HK
dc.publisherFrontiers in Bioscience. The Journal's web site is located at http://www.frontbiosci.org/en_HK
dc.relation.ispartofFrontiers in Bioscienceen_HK
dc.subjectCanceren_HK
dc.subjectChromosomal instabilityen_HK
dc.subjectGenomic instabilityen_HK
dc.subjectReviewen_HK
dc.subjectTelomereen_HK
dc.titleTelomere dysfunction, genome instability and canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1093-9946&volume=13&spage=2075&epage=2090&date=2008&atitle=Telomere+dysfunction,+genome+instability+and+canceren_HK
dc.identifier.emailCheung, ALM: lmcheung@hku.hken_HK
dc.identifier.emailDeng, W: wdeng@hkucc.hku.hken_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.identifier.authorityDeng, W=rp01640en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2741/2825en_HK
dc.identifier.scopuseid_2-s2.0-38449085735en_HK
dc.identifier.hkuros141225en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-38449085735&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume13en_HK
dc.identifier.issue6en_HK
dc.identifier.spage2075en_HK
dc.identifier.epage2090en_HK
dc.identifier.isiWOS:000255775700169-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK
dc.identifier.scopusauthoridDeng, W=7202223673en_HK

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