Update on the clinical use of kinase inhibitors in melanoma

J Dtsch Dermatol Ges. 2017 Sep;15(9):887-893. doi: 10.1111/ddg.13321.

Abstract

The identification of targetable molecules in cellular signaling pathways represents a milestone in the treatment of melanoma. Selective inhibitors of these molecules, known as phosphokinases, allow for individual signaling pathways to be "switched off". This is of particular importance for tumors in which these pathways are constitutively activated by mutations in genes encoding said molecules. Especially patients with BRAF-mutated melanomas significantly benefit from kinase inhibitor therapies, with the current standard of combined BRAF and MEK inhibition providing very good long-term disease control. Such regimens have been shown to achieve a progression-free survival of more than ten months and an overall survival of more than two years, along with good quality of life. Given that the majority of patients develop secondary resistance during long-term kinase inhibitor therapy, current clinical trials are geared towards finding suitable drug combinations including inhibitors of other signaling pathways as well as immune checkpoint inhibitors. The present review highlights targeted therapies for melanoma currently available as well as potential future options presently under clinical investigation.

Publication types

  • Review

MeSH terms

  • Clinical Trials as Topic
  • DNA Mutational Analysis
  • Disease-Free Survival
  • Drug Therapy, Combination
  • GTP Phosphohydrolases / antagonists & inhibitors
  • GTP Phosphohydrolases / genetics
  • Humans
  • Melanoma / drug therapy*
  • Melanoma / genetics
  • Melanoma / mortality
  • Membrane Proteins / antagonists & inhibitors
  • Membrane Proteins / genetics
  • Protein Kinase Inhibitors / therapeutic use*
  • Proto-Oncogene Proteins B-raf / antagonists & inhibitors
  • Proto-Oncogene Proteins B-raf / genetics
  • Proto-Oncogene Proteins c-kit / antagonists & inhibitors
  • Proto-Oncogene Proteins c-kit / genetics
  • Signal Transduction / drug effects
  • Signal Transduction / genetics
  • Skin Neoplasms / drug therapy*
  • Skin Neoplasms / genetics
  • Skin Neoplasms / mortality
  • Treatment Outcome

Substances

  • Membrane Proteins
  • Protein Kinase Inhibitors
  • Proto-Oncogene Proteins c-kit
  • BRAF protein, human
  • Proto-Oncogene Proteins B-raf
  • GTP Phosphohydrolases
  • NRAS protein, human