BRAF(E600) in benign and malignant human tumours

Oncogene. 2008 Feb 7;27(7):877-95. doi: 10.1038/sj.onc.1210704. Epub 2007 Aug 27.


Of the RAF family of protein kinases, BRAF is the only member to be frequently activated by mutation in cancer. A single amino acid substitution (V600E) accounts for the vast majority and results in constitutive activation of BRAF kinase function. Its expression is required to maintain the proliferative and oncogenic characteristics of BRAF(E600)-expressing human tumour cells. Although BRAF(E600) acts as an oncogene in the context of additional genetic lesions, in primary cells it appears to be associated rather with transient stimulation of proliferation. Eventually, BRAF(E600) signalling triggers cell cycle arrest with the hallmarks of cellular senescence, as is illustrated by several recent studies in cultured cells, animal models and benign human lesions. In this review, we will discuss recent advances in our understanding of the role of BRAF(E600) in benign and malignant human tumours and the implications for therapeutic intervention.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Proliferation
  • Humans
  • Neoplasms / metabolism*
  • Neoplasms / therapy
  • Proto-Oncogene Proteins B-raf / physiology*
  • Signal Transduction


  • Proto-Oncogene Proteins B-raf