| Telomere recombination and alternative telomere lengthening mechanisms. | |
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MedLine Citation:
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PMID: 23276906 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Telomeres are nucleoprotein structures at the ends of linear chromosomes that protect them from being recognized as DNA double stranded breaks. Telomeres shorten with every cell division and in the absence of the checkpoint mechanisms critical telomere shortening leads to chromosome end fusions and genomic instability. Cancer cells achieve immortality by engaging in one of the two known mechanisms for telomere maintenance: elongation by telomerase or through recombination. Recombination based elongation of telomeres, also known as alternative lengthening of telomeres or ALT, is prevalent among cancers of mesenchymal origin. However, the conditions favoring ALT emergence are not known. Here we will discuss possible players in ALT mechanisms, including recruitment of telomeres to recombination centers, alterations of telomere associated proteins and modifications at the level of chromatin that could generate recombination permissive conditions at telomeres. |
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Authors:
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Irena Draskovic; Arturo Londono-Vallejo |
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Publication Detail:
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Type: Journal Article Date: 2013-01-01 |
Journal Detail:
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Title: Frontiers in bioscience : a journal and virtual library Volume: 18 ISSN: 1093-4715 ISO Abbreviation: Front. Biosci. Publication Date: 2013 |
Date Detail:
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Created Date: 2013-01-01 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9709506 Medline TA: Front Biosci Country: United States |
Other Details:
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Languages: eng Pagination: 1-20 Citation Subset: IM |
Affiliation:
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Institut Curie, Centre de recherche, 75005 Paris, France. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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