Tyrosine kinase mutations in human cancer

Curr Mol Med. 2007 Feb;7(1):77-84. doi: 10.2174/156652407779940486.

Abstract

A subset of tyrosine kinases are activated by mutations which contribute to the malignant transformation, growth, and metastasis of human cancers. Mutations change the expression, conformation and/or stability of tyrosine kinases, often leading to constitutive activation of the signaling pathways the kinases regulate. Given that tyrosine kinases are key members of signaling cascades, mutations have multiple effects on various cellular proteins. This review will focus on four kinases (EGFR, c-Met, c-Kit, and PI3-kinase) known to be mutated in human cancer. It will discuss the effects that these mutations have on the biology of tumors, and how our understanding of the structure and function of kinases and their mutations is currently being used to design targeted treatments.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • ErbB Receptors / genetics
  • Humans
  • Mutation / genetics*
  • Neoplasms / enzymology*
  • Neoplasms / genetics*
  • Neoplasms / therapy
  • Phosphatidylinositol 3-Kinases / genetics
  • Protein-Tyrosine Kinases / genetics*
  • Protein-Tyrosine Kinases / metabolism
  • Proto-Oncogene Proteins c-kit / genetics
  • Proto-Oncogene Proteins c-met / genetics

Substances

  • Phosphatidylinositol 3-Kinases
  • ErbB Receptors
  • Protein-Tyrosine Kinases
  • Proto-Oncogene Proteins c-kit
  • Proto-Oncogene Proteins c-met