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The G(1 )phase Cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification
Because centrosome amplification generates aneuploidy and since centrosome amplification is ubiquitous in human tumors, a strong case is made for centrosome amplification being a major force in tumor biogenesis. Various evidence showing that oncogenes and altered tumor suppressors lead to centrosome...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2011
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3038874/ https://www.ncbi.nlm.nih.gov/pubmed/21272329 http://dx.doi.org/10.1186/1747-1028-6-2 |
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author | Harrison, Mary K Adon, Arsene M Saavedra, Harold I |
author_facet | Harrison, Mary K Adon, Arsene M Saavedra, Harold I |
author_sort | Harrison, Mary K |
collection | PubMed |
description | Because centrosome amplification generates aneuploidy and since centrosome amplification is ubiquitous in human tumors, a strong case is made for centrosome amplification being a major force in tumor biogenesis. Various evidence showing that oncogenes and altered tumor suppressors lead to centrosome amplification and aneuploidy suggests that oncogenes and altered tumor suppressors are a major source of genomic instability in tumors, and that they generate those abnormal processes to initiate and sustain tumorigenesis. We discuss how altered tumor suppressors and oncogenes utilize the cell cycle regulatory machinery to signal centrosome amplification and aneuploidy. |
format | Text |
id | pubmed-3038874 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-30388742011-02-15 The G(1 )phase Cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification Harrison, Mary K Adon, Arsene M Saavedra, Harold I Cell Div Review Because centrosome amplification generates aneuploidy and since centrosome amplification is ubiquitous in human tumors, a strong case is made for centrosome amplification being a major force in tumor biogenesis. Various evidence showing that oncogenes and altered tumor suppressors lead to centrosome amplification and aneuploidy suggests that oncogenes and altered tumor suppressors are a major source of genomic instability in tumors, and that they generate those abnormal processes to initiate and sustain tumorigenesis. We discuss how altered tumor suppressors and oncogenes utilize the cell cycle regulatory machinery to signal centrosome amplification and aneuploidy. BioMed Central 2011-01-27 /pmc/articles/PMC3038874/ /pubmed/21272329 http://dx.doi.org/10.1186/1747-1028-6-2 Text en Copyright ©2011 Harrison et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Harrison, Mary K Adon, Arsene M Saavedra, Harold I The G(1 )phase Cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification |
title | The G(1 )phase Cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification |
title_full | The G(1 )phase Cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification |
title_fullStr | The G(1 )phase Cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification |
title_full_unstemmed | The G(1 )phase Cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification |
title_short | The G(1 )phase Cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification |
title_sort | g(1 )phase cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3038874/ https://www.ncbi.nlm.nih.gov/pubmed/21272329 http://dx.doi.org/10.1186/1747-1028-6-2 |
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