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A reason why the ERBB2 gene is amplified and not mutated in breast cancer

Alterations of receptor-type tyrosine kinases (RTK) are frequent in human cancers. They can result from translocation, mutation or amplification. The ERBB2 RTK is encoded by a gene that is amplified in about 20% breast cancers. The question is: why is this RTK specifically subjected to this type of...

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Detalles Bibliográficos
Autores principales: Birnbaum, Daniel, Sircoulomb, Fabrice, Imbert, Jean
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2649042/
https://www.ncbi.nlm.nih.gov/pubmed/19226453
http://dx.doi.org/10.1186/1475-2867-9-5
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author Birnbaum, Daniel
Sircoulomb, Fabrice
Imbert, Jean
author_facet Birnbaum, Daniel
Sircoulomb, Fabrice
Imbert, Jean
author_sort Birnbaum, Daniel
collection PubMed
description Alterations of receptor-type tyrosine kinases (RTK) are frequent in human cancers. They can result from translocation, mutation or amplification. The ERBB2 RTK is encoded by a gene that is amplified in about 20% breast cancers. The question is: why is this RTK specifically subjected to this type of alteration? We propose that ERBB2 gene amplification is used to overcome repression of its expression by sequence-specific transcription factors.
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spelling pubmed-26490422009-02-28 A reason why the ERBB2 gene is amplified and not mutated in breast cancer Birnbaum, Daniel Sircoulomb, Fabrice Imbert, Jean Cancer Cell Int Hypothesis Alterations of receptor-type tyrosine kinases (RTK) are frequent in human cancers. They can result from translocation, mutation or amplification. The ERBB2 RTK is encoded by a gene that is amplified in about 20% breast cancers. The question is: why is this RTK specifically subjected to this type of alteration? We propose that ERBB2 gene amplification is used to overcome repression of its expression by sequence-specific transcription factors. BioMed Central 2009-02-18 /pmc/articles/PMC2649042/ /pubmed/19226453 http://dx.doi.org/10.1186/1475-2867-9-5 Text en Copyright © 2009 Birnbaum 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 Hypothesis
Birnbaum, Daniel
Sircoulomb, Fabrice
Imbert, Jean
A reason why the ERBB2 gene is amplified and not mutated in breast cancer
title A reason why the ERBB2 gene is amplified and not mutated in breast cancer
title_full A reason why the ERBB2 gene is amplified and not mutated in breast cancer
title_fullStr A reason why the ERBB2 gene is amplified and not mutated in breast cancer
title_full_unstemmed A reason why the ERBB2 gene is amplified and not mutated in breast cancer
title_short A reason why the ERBB2 gene is amplified and not mutated in breast cancer
title_sort reason why the erbb2 gene is amplified and not mutated in breast cancer
topic Hypothesis
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2649042/
https://www.ncbi.nlm.nih.gov/pubmed/19226453
http://dx.doi.org/10.1186/1475-2867-9-5
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