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Telomore dysfunction and cancer

DC FieldValueLanguage
dc.contributor.author이옥희-
dc.contributor.author허지회-
dc.date.accessioned2015-04-23T16:38:07Z-
dc.date.available2015-04-23T16:38:07Z-
dc.date.issued2010-
dc.identifier.issn1226-0165-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/100942-
dc.description.abstractUnlike the circular structure of prokaryotic chromosome, the structure of eukaryotic chromosomes is linear. To prevent the ends of linear chromosomes from being recognized as double-stranded DNA breaks by DNA damage, chromosome end is capped by the special chromatin structure, telomere. Telomere in vertebrate consists of TTAGGG tandem repeats and telosome/shelterin complex including TRF1, TRF2, RAP1, TIN2, TPP1, and POT1. The average length of human telomere is 10∼15 kb at birth, and several rounds of cell division lead to telomere shortening in somatic cells due to the absence of telomerase, a reverse transcriptase, adding TTAGGG repeats at chromosome ends. The uncapping telomere by telomere attrition causes genomic instability activating cell cycle checkpoints and inducing cell cycle arrest, senescence, or apoptosis. Highly-proliferative tumor cells that have the impaired checkpoints and short telomeres can escape normal limits on cell proliferation, resulting in massive genome instability and malignancy of tumor cells. In this review, we provide an overview of telomere structure and function, and the relationship between telomere dysfunction and the initiation of human cancer-
dc.description.statementOfResponsibilityopen-
dc.format.extent28~33-
dc.relation.isPartOfCancer Prevention Research-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleTelomore dysfunction and cancer-
dc.typeArticle-
dc.contributor.collegeResearcher Institutes (부설 연구소)-
dc.contributor.departmentYonsei Integrative Research Institute for Cerebral & Cardiovascular Disease (뇌심혈관질환융합연구사업단)-
dc.contributor.googleauthorYoungsok Choi-
dc.contributor.googleauthorHyunji Lee-
dc.contributor.googleauthorJi Hoe Heo-
dc.contributor.googleauthorOk-Hee Lee-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02970-
dc.contributor.localIdA04369-
dc.relation.journalcodeJ00451-
dc.contributor.alternativeNameLee, Ok Hee-
dc.contributor.alternativeNameHeo, Ji Hoe-
dc.contributor.affiliatedAuthorLee, Ok Hee-
dc.contributor.affiliatedAuthorHeo, Ji Hoe-
dc.citation.volume15-
dc.citation.number1-
dc.citation.startPage28-
dc.citation.endPage33-
dc.identifier.bibliographicCitationCancer Prevention Research, Vol.15(1) : 28-33, 2010-
Appears in Collections:
5. Research Institutes (연구소) > Yonsei Integrative Research Institute for Cerebral & Cardiovascular Disease (뇌심혈관질환융합연구사업단) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers

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