Targeting the Raf/MEK/ERK pathway with small-molecule inhibitors

J. A. McCubrey, M. Milella, A. Tafuri, A. M. Martelli, P. Lunghi, A. Bonati, M. Cervello, J. T. Lee, L. S. Steelman

Research output: Contribution to journalArticlepeer-review


Mutations occur in some cancer cells and result in elevated expression or constitutive activation of various growth factor receptors. The Raf/MEK/ERK pathway is often activated by mutations in these growth factor receptors. This pathway is regulated by upstream Ras, which is mutated in 20 to 30% of human cancers. B-Raf is also activated by mutation, especially in melanoma and thyroid cancers. Many of the events elicited by the Raf/MEK/ERK pathway have direct effects on survival and proliferative pathways. Aberrant regulation of the Raf/MEK/ERK pathway can contribute to uncontrolled cell growth and lead to malignant transformation. The effective targeting of this pathway may result in the suppression of cell growth, and death of malignant cells. This review focuses on targeting the Raf/MEK/ERK pathway with small-molecule inhibitors for the treatment of cancer.

Original languageEnglish
Pages (from-to)614-630
Number of pages17
JournalCurrent Opinion in Investigational Drugs
Issue number6
Publication statusPublished - Jun 2008


  • Apoptosis
  • Cancer
  • ERK
  • Inhibitor
  • MEK
  • Raf
  • Signal transduction

ASJC Scopus subject areas

  • Pharmacology


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