Incidence of the V600K mutation among melanoma patients with BRAF mutations, and potential therapeutic response to the specific BRAF inhibitor PLX4032

Journal of Translational Medicine

Commentary

Elaine Cheng¹  Antonella Bacchiocchi¹  Ruth Halaban¹  Anna C Pavlick²  Jill C Rubinstein³  Stephan Ariyan⁴  Deepak Narayan⁴  Mario Sznol⁵  Harriet M Kluger⁵ 

[1] Department of Dermatology, Yale University School of Medicine, 06520, New Haven, CT, USA;Department of Medical Oncology, New York University, 10016, New York City, New York, USA;Department of Pathology, Yale University School of Medicine, 06520, New Haven, CT, USA;Plastic and Reconstructive Surgery, Yale University School of Medicine, 06520, New Haven, CT, USA;Section of Medical Oncology, Yale University School of Medicine, 06520, New Haven, CT, USA;

关键词: Melanoma;    Melanoma Patient;    BRAF Mutation;    Imiquimod;    BRAF V600E Mutation;   

DOI  :  10.1186/1479-5876-8-67

 received in 2010-05-12, accepted in 2010-07-14,  发布年份 2010

来源: Springer

【 摘 要 】

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.

【 授权许可】

Unknown   
© Rubinstein et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. 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.