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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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Autores principales: Harrison, Mary K, Adon, Arsene M, Saavedra, Harold I
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
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.
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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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