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A STATement on Vemurafenib-Resistant Melanoma
Despite recent advancements in the treatment of late-stage mutant BRAF (V600E/K) melanomas, a major hurdle continues to be acquired resistance to BRAF inhibitors such as Vemurafenib. The mechanisms for resistance have proven to be heterogeneous, emphasizing the need to utilize broad therapeutic appr...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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2013
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3713534/ https://www.ncbi.nlm.nih.gov/pubmed/23856932 http://dx.doi.org/10.1038/jid.2013.136 |
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author | Hartsough, Edward J. Aplin, Andrew E. |
author_facet | Hartsough, Edward J. Aplin, Andrew E. |
author_sort | Hartsough, Edward J. |
collection | PubMed |
description | Despite recent advancements in the treatment of late-stage mutant BRAF (V600E/K) melanomas, a major hurdle continues to be acquired resistance to BRAF inhibitors such as Vemurafenib. The mechanisms for resistance have proven to be heterogeneous, emphasizing the need to utilize broad therapeutic approachs. The present study, “Stat3 targeted therapies overcome the acquired resistance to vemurafenib in melanomas” by Liu et al., proposes that STAT3-PAX3 signaling may be a mechanism that is utilized by melanomas to resist RAF inhibitors. |
format | Online Article Text |
id | pubmed-3713534 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
record_format | MEDLINE/PubMed |
spelling | pubmed-37135342014-02-01 A STATement on Vemurafenib-Resistant Melanoma Hartsough, Edward J. Aplin, Andrew E. J Invest Dermatol Article Despite recent advancements in the treatment of late-stage mutant BRAF (V600E/K) melanomas, a major hurdle continues to be acquired resistance to BRAF inhibitors such as Vemurafenib. The mechanisms for resistance have proven to be heterogeneous, emphasizing the need to utilize broad therapeutic approachs. The present study, “Stat3 targeted therapies overcome the acquired resistance to vemurafenib in melanomas” by Liu et al., proposes that STAT3-PAX3 signaling may be a mechanism that is utilized by melanomas to resist RAF inhibitors. 2013-08 /pmc/articles/PMC3713534/ /pubmed/23856932 http://dx.doi.org/10.1038/jid.2013.136 Text en http://www.nature.com/authors/editorial_policies/license.html#terms Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms |
spellingShingle | Article Hartsough, Edward J. Aplin, Andrew E. A STATement on Vemurafenib-Resistant Melanoma |
title | A STATement on Vemurafenib-Resistant Melanoma |
title_full | A STATement on Vemurafenib-Resistant Melanoma |
title_fullStr | A STATement on Vemurafenib-Resistant Melanoma |
title_full_unstemmed | A STATement on Vemurafenib-Resistant Melanoma |
title_short | A STATement on Vemurafenib-Resistant Melanoma |
title_sort | statement on vemurafenib-resistant melanoma |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3713534/ https://www.ncbi.nlm.nih.gov/pubmed/23856932 http://dx.doi.org/10.1038/jid.2013.136 |
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