Targeting BRAF in advanced melanoma: a first step toward manageable disease

Clin Cancer Res. 2011 Apr 1;17(7):1658-63. doi: 10.1158/1078-0432.CCR-10-0174. Epub 2011 Mar 29.

Abstract

Melanoma is the deadliest form of skin cancer and its incidence has been increasing worldwide. The disease manifests itself as clinically and genetically distinct subgroups, indicating the need for patient-specific diagnostic and treatment tools. The discovery of activating mutations (V600E) in the BRAF kinase in approximately 50% of patients spurred the development of compounds to inhibit aberrant BRAF activity, and the first drug candidate to show promising clinical activity is PLX4032 (also known as RG7204). Most recent clinical data from a phase II trial indicate that PLX4032 causes tumor regression and stabilized disease in >50% of advanced melanoma patients harboring BRAF V600E tumors. These data validate the effectiveness of oncogene-targeted therapy against advanced melanoma and offer hope that the disease can be overcome. However, as melanoma is dynamic and heterogeneous, careful treatment strategies and combination therapies are warranted to obtain long-term clinical effects.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Humans
  • Indoles / pharmacology
  • Indoles / therapeutic use
  • Melanoma / drug therapy
  • Melanoma / metabolism*
  • Melanoma / pathology
  • Mutation
  • Proto-Oncogene Proteins B-raf / antagonists & inhibitors
  • Proto-Oncogene Proteins B-raf / genetics
  • Proto-Oncogene Proteins B-raf / metabolism*
  • Skin Neoplasms / drug therapy
  • Skin Neoplasms / metabolism*
  • Skin Neoplasms / pathology
  • Sulfonamides / pharmacology
  • Sulfonamides / therapeutic use
  • Vemurafenib

Substances

  • Antineoplastic Agents
  • Indoles
  • Sulfonamides
  • Vemurafenib
  • BRAF protein, human
  • Proto-Oncogene Proteins B-raf