1. Incidence of the V600K mutation among melanoma patients with BRAF mutations, and potential therapeutic response to the specific BRAF inhibitor PLX4032
- Author
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Mario Sznol, Harriet M. Kluger, Elaine Cheng, Antonella Bacchiocchi, Jill C. Rubinstein, Anna C. Pavlick, Deepak Narayan, Ruth Halaban, and Stephan Ariyan
- Subjects
BRAF inhibitor ,endocrine system diseases ,lcsh:Medicine ,Biology ,General Biochemistry, Genetics and Molecular Biology ,Proto-Oncogene Proteins B-raf ,03 medical and health sciences ,0302 clinical medicine ,medicine ,neoplasms ,030304 developmental biology ,Medicine(all) ,0303 health sciences ,Kinase ,Biochemistry, Genetics and Molecular Biology(all) ,Incidence (epidemiology) ,Melanoma ,lcsh:R ,General Medicine ,medicine.disease ,digestive system diseases ,3. Good health ,Clinical trial ,030220 oncology & carcinogenesis ,Mutation (genetic algorithm) ,Cancer research ,Commentary ,V600E - Abstract
Activating mutations in BRAF kinase are common in melanomas. Clinical trials with PLX4032, the mutant-BRAF inhibitor, show promising preliminary results in patients selected for the presence of V600E mutation. However, activating V600K mutation is the other most common mutation, yet patients with this variant are currently excluded from the PLX4032 trials. Here we present evidence that a patient bearing the BRAF V600K mutation responded remarkably to PLX4032, suggesting that clinical trials should include all patients with activating BRAF V600E/K mutations.
- Published
- 2010