There are no currently approved targeted therapies for BRAF wild-type melanoma patients harboring NRAS driver mutations though an array of agents are in early phase clinical trials. The diverse strategies taken exploit combined MAP kinase signaling blockade with inhibition of cell cycle mediators, inhibition of the autophagy pathway, and alteration of kinases involved in actin cytoskeleton signaling. Future advances of developmental therapeutics into late stage trials may yield new options beyond immunotherapy for patients with advanced stage disease and NRAS mutation status.
Keyphrases
- wild type
- cell cycle
- clinical trial
- end stage renal disease
- cell proliferation
- ejection fraction
- chronic kidney disease
- newly diagnosed
- cell death
- oxidative stress
- prognostic factors
- small molecule
- endoplasmic reticulum stress
- high resolution
- peritoneal dialysis
- signaling pathway
- high throughput
- tyrosine kinase
- high density
- single cell
- phase ii
- smoking cessation
- study protocol
- mass spectrometry