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Goldinger SM, Murer C, Stieger P, et al. Targeted therapy in melanoma - the role of BRAF, RAS and KIT mutations. EJC Suppl. 2013;11(2):92-6doi: 10.1016/j.ejcsup.2013.07.011.
Goldinger, S. M., Murer, C., Stieger, P., & Dummer, R. (2013). Targeted therapy in melanoma - the role of BRAF, RAS and KIT mutations. EJC supplements : EJC : official journal of EORTC, European Organization for Research and Treatment of Cancer ... [et al.], 11(2), 92-6. https://doi.org/10.1016/j.ejcsup.2013.07.011
Goldinger, Simone M, et al. "Targeted therapy in melanoma - the role of BRAF, RAS and KIT mutations." EJC supplements : EJC : official journal of EORTC, European Organization for Research and Treatment of Cancer ... [et al.] vol. 11,2 (2013): 92-6. doi: https://doi.org/10.1016/j.ejcsup.2013.07.011
Goldinger SM, Murer C, Stieger P, Dummer R. Targeted therapy in melanoma - the role of BRAF, RAS and KIT mutations. EJC Suppl. 2013 Sep;11(2):92-6. doi: 10.1016/j.ejcsup.2013.07.011. PMID: 26217117; PMCID: PMC4041182.
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EJC Suppl. 2013 Sep;11(2):92-6. doi: 10.1016/j.ejcsup.2013.07.011.

Targeted therapy in melanoma - the role of BRAF, RAS and KIT mutations.

EJC supplements : EJC : official journal of EORTC, European Organization for Research and Treatment of Cancer ... [et al.]

Simone M Goldinger, Carla Murer, Pascale Stieger, Reinhard Dummer

Affiliations

  1. University Hospital, Department of Dermatology, Zurich, Switzerland.

PMID: 26217117 PMCID: PMC4041182 DOI: 10.1016/j.ejcsup.2013.07.011

Abstract

Melanoma today is considered as a spectrum of melanocytic malignancies characterised by clinical and molecular features, including targetable mutations in several kinases such as BRAF or c-KIT. The successful development of therapies targeting these mutations has resulted in new specific treatment options. These include vemurafenib, dabrafenib, trametinib, imatinib and other kinase inhibitors that are selected when the respective mutation is present. The BRAF inhibitor vemurafenib has resulted in improved survival in patients with BRAF-mutated advanced melanoma. Dabrafenib has shown similar efficacy. The MEK inhibitor trametinib also improved overall survival. In addition, the MEK inhibitor MEK 162 was investigated in a phase II clinical trial and showed promising efficacy in terms of response rate and progression-free survival (PFS) in NRAS-mutated melanomas. After this first success in the treatment of advanced melanoma, there is expectation that combinations of kinase inhibitors will additionally improve overall survival rates and PFS in advanced melanoma.

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