Towards a unified model of RAF inhibitor resistance Academic Article uri icon

Overview

MeSH Major

  • Antineoplastic Agents
  • Drug Resistance, Neoplasm
  • Extracellular Signal-Regulated MAP Kinases
  • Melanoma
  • Proto-Oncogene Proteins B-raf
  • Skin Neoplasms

abstract

  • ATP-competitive RAF inhibitors elicit profound but often temporary antitumor responses in patients with BRAF-mutant melanoma. Analysis of tumor samples collected at the time of disease progression indicates that alterations within the extracellular signal-regulated kinase (ERK) pathway that result in reactivation of ERK signaling are present in most patients. Mutations in the phosphoinositide 3-kinase/AKT pathway that enhance the adaptive response to RAF inhibitors also contribute to RAF inhibitor resistance in a subset of patients.

publication date

  • January 2014

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC4986142

Digital Object Identifier (DOI)

  • 10.1158/2159-8290.cd-13-0961

PubMed ID

  • 24402945

Additional Document Info

start page

  • 27

end page

  • 30

volume

  • 4

number

  • 1