Old Habits Die Hard: Addiction of BRAF-Mutant Cancer Cells to MAP Kinase Signaling

Cancer Discov. 2015 Apr;5(4):348-50. doi: 10.1158/2159-8290.CD-15-0221.

Abstract

Dual and triple combination therapies with RAF inhibitors plus other targeted agents have demonstrated promising clinical utility in BRAFV600-mutant solid tumors. However, despite vertical inhibition at multiple nodes on the MAPK signaling pathway, resistant tumors emerge. Ahronian and colleagues show that in BRAF-mutant colorectal cancer, resistance involves reactivation of RAS/RAF/MEK/ERK signaling and may be overcome by newly emerging ERK inhibitors.

Publication types

  • Research Support, N.I.H., Extramural
  • Comment

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms / metabolism*
  • Drug Resistance, Neoplasm / drug effects*
  • Humans
  • MAP Kinase Signaling System / drug effects*
  • Mutation*
  • Protein Kinase Inhibitors / pharmacology*
  • Proto-Oncogene Proteins B-raf / genetics*

Substances

  • Antineoplastic Agents
  • Protein Kinase Inhibitors
  • Proto-Oncogene Proteins B-raf