Abstract |
Melanoma is resistant to cytotoxic therapy, and treatment options for advanced disease have been limited historically. However, improved understanding of melanoma driver mutations, particularly those involving the mitogen-activated protein kinase pathway, has led to the development of targeted therapies that are effective in this previously treatment-refractory disease. In cutaneous melanomas with BRAF V600 mutations the selective RAF inhibitors, vemurafenib and dabrafenib, and the MEK inhibitor, trametinib, have demonstrated survival benefits. Early signals of efficacy have also been demonstrated with MEK inhibitors in melanomas with NRAS mutations, and KIT inhibitors offer promise in melanomas driven through activation of their target receptor.
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Authors | Damien Kee, Grant McArthur |
Journal | Hematology/oncology clinics of North America
(Hematol Oncol Clin North Am)
Vol. 28
Issue 3
Pg. 491-505
(Jun 2014)
ISSN: 1558-1977 [Electronic] United States |
PMID | 24880943
(Publication Type: Journal Article, Review)
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Copyright | Copyright © 2014 Elsevier Inc. All rights reserved. |
Chemical References |
- Imidazoles
- Indoles
- Oximes
- Protein Kinase Inhibitors
- Sulfonamides
- Vemurafenib
- BRAF protein, human
- Proto-Oncogene Proteins B-raf
- dabrafenib
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Topics |
- Humans
- Imidazoles
(therapeutic use)
- Indoles
(therapeutic use)
- Melanoma
(drug therapy, genetics)
- Molecular Targeted Therapy
(methods)
- Mutation
- Oximes
(therapeutic use)
- Protein Kinase Inhibitors
(therapeutic use)
- Proto-Oncogene Proteins B-raf
(antagonists & inhibitors, genetics)
- Skin Neoplasms
(drug therapy, genetics)
- Sulfonamides
(therapeutic use)
- Survival Analysis
- Vemurafenib
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