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Revisiting Telomere Shortening in Cancer
Telomeres, the protective structures of chromosome ends are gradually shortened by each cell division, eventually leading to senescence or apoptosis. Cancer cells maintain the telomere length for unlimited growth by telomerase reactivation or a recombination-based mechanism. Recent genome-wide analy...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6406355/ https://www.ncbi.nlm.nih.gov/pubmed/30709063 http://dx.doi.org/10.3390/cells8020107 |
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author | Okamoto, Keiji Seimiya, Hiroyuki |
author_facet | Okamoto, Keiji Seimiya, Hiroyuki |
author_sort | Okamoto, Keiji |
collection | PubMed |
description | Telomeres, the protective structures of chromosome ends are gradually shortened by each cell division, eventually leading to senescence or apoptosis. Cancer cells maintain the telomere length for unlimited growth by telomerase reactivation or a recombination-based mechanism. Recent genome-wide analyses have unveiled genetic and epigenetic alterations of the telomere maintenance machinery in cancer. While telomerase inhibition reveals that longer telomeres are more advantageous for cell survival, cancer cells often have paradoxically shorter telomeres compared with those found in the normal tissues. In this review, we summarize the latest knowledge about telomere length alterations in cancer and revisit its rationality. Finally, we discuss the potential utility of telomere length as a prognostic biomarker. |
format | Online Article Text |
id | pubmed-6406355 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-64063552019-03-19 Revisiting Telomere Shortening in Cancer Okamoto, Keiji Seimiya, Hiroyuki Cells Review Telomeres, the protective structures of chromosome ends are gradually shortened by each cell division, eventually leading to senescence or apoptosis. Cancer cells maintain the telomere length for unlimited growth by telomerase reactivation or a recombination-based mechanism. Recent genome-wide analyses have unveiled genetic and epigenetic alterations of the telomere maintenance machinery in cancer. While telomerase inhibition reveals that longer telomeres are more advantageous for cell survival, cancer cells often have paradoxically shorter telomeres compared with those found in the normal tissues. In this review, we summarize the latest knowledge about telomere length alterations in cancer and revisit its rationality. Finally, we discuss the potential utility of telomere length as a prognostic biomarker. MDPI 2019-01-31 /pmc/articles/PMC6406355/ /pubmed/30709063 http://dx.doi.org/10.3390/cells8020107 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Okamoto, Keiji Seimiya, Hiroyuki Revisiting Telomere Shortening in Cancer |
title | Revisiting Telomere Shortening in Cancer |
title_full | Revisiting Telomere Shortening in Cancer |
title_fullStr | Revisiting Telomere Shortening in Cancer |
title_full_unstemmed | Revisiting Telomere Shortening in Cancer |
title_short | Revisiting Telomere Shortening in Cancer |
title_sort | revisiting telomere shortening in cancer |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6406355/ https://www.ncbi.nlm.nih.gov/pubmed/30709063 http://dx.doi.org/10.3390/cells8020107 |
work_keys_str_mv | AT okamotokeiji revisitingtelomereshorteningincancer AT seimiyahiroyuki revisitingtelomereshorteningincancer |