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BRAF Mutation in Colorectal Cancer: An Update

Colorectal cancer (CRC) is still one of the deadliest cancer-related diseases. About 10% of CRC patients are characterized by a mutation in the B-Raf proto-oncogene serine/threonine kinase (BRAF) gene resulting in a valine-to-glutamate change at the residue 600 (V600E). This mutation is also present...

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Detalles Bibliográficos
Autor principal: Barras, David
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Libertas Academica 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4562608/
https://www.ncbi.nlm.nih.gov/pubmed/26396549
http://dx.doi.org/10.4137/BIC.S25248
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author Barras, David
author_facet Barras, David
author_sort Barras, David
collection PubMed
description Colorectal cancer (CRC) is still one of the deadliest cancer-related diseases. About 10% of CRC patients are characterized by a mutation in the B-Raf proto-oncogene serine/threonine kinase (BRAF) gene resulting in a valine-to-glutamate change at the residue 600 (V600E). This mutation is also present in more than 60% of melanoma patients. BRAF inhibitors were developed and found to improve patient survival; however, most patients at the end of the track ultimately develop resistance to these inhibitors. Melanoma patients benefit from the combination of BRAF inhibitors with mitogen/extracellular signal-regulated kinase (MEK) inhibitors, among others. Unfortunately, colorectal patients do not respond much efficiently, which suggests different resistance mechanisms between the two cancer types. This review aims at shedding light on recent discoveries that improve our understanding of the BRAF mutation biology in CRC.
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spelling pubmed-45626082015-09-22 BRAF Mutation in Colorectal Cancer: An Update Barras, David Biomark Cancer Review Colorectal cancer (CRC) is still one of the deadliest cancer-related diseases. About 10% of CRC patients are characterized by a mutation in the B-Raf proto-oncogene serine/threonine kinase (BRAF) gene resulting in a valine-to-glutamate change at the residue 600 (V600E). This mutation is also present in more than 60% of melanoma patients. BRAF inhibitors were developed and found to improve patient survival; however, most patients at the end of the track ultimately develop resistance to these inhibitors. Melanoma patients benefit from the combination of BRAF inhibitors with mitogen/extracellular signal-regulated kinase (MEK) inhibitors, among others. Unfortunately, colorectal patients do not respond much efficiently, which suggests different resistance mechanisms between the two cancer types. This review aims at shedding light on recent discoveries that improve our understanding of the BRAF mutation biology in CRC. Libertas Academica 2015-09-06 /pmc/articles/PMC4562608/ /pubmed/26396549 http://dx.doi.org/10.4137/BIC.S25248 Text en © 2015 the author(s), publisher and licensee Libertas Academica Ltd. This is an open-access article distributed under the terms of the Creative Commons CC-BY-NC 3.0 License.
spellingShingle Review
Barras, David
BRAF Mutation in Colorectal Cancer: An Update
title BRAF Mutation in Colorectal Cancer: An Update
title_full BRAF Mutation in Colorectal Cancer: An Update
title_fullStr BRAF Mutation in Colorectal Cancer: An Update
title_full_unstemmed BRAF Mutation in Colorectal Cancer: An Update
title_short BRAF Mutation in Colorectal Cancer: An Update
title_sort braf mutation in colorectal cancer: an update
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4562608/
https://www.ncbi.nlm.nih.gov/pubmed/26396549
http://dx.doi.org/10.4137/BIC.S25248
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