[Kinase inhibitors]

Nihon Rinsho. 2010 Jun;68(6):1059-66.
[Article in Japanese]

Abstract

Various kinases phosphorylate their substrates and thereby switch on or off their functions. Dysregulation of kinases that regulate cell growth signals induces carcinogenesis or malignant phenotypes in cancer. Therefore, kinases are considered to be most promising therapeutic targets in cancer treatment, and the development of kinase inhibitors has been the most hot area. In this article, the present status and the perspective of kinase inhibitors were described.

Publication types

  • Review

MeSH terms

  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Humanized
  • Antibodies, Monoclonal, Murine-Derived
  • Benzamides
  • Bevacizumab
  • Biomarkers, Tumor
  • Drug Design
  • ErbB Receptors / antagonists & inhibitors
  • Fusion Proteins, bcr-abl / antagonists & inhibitors
  • Genes, ras / genetics
  • Humans
  • Imatinib Mesylate
  • Mutation
  • Neoplasms / diagnosis
  • Neoplasms / drug therapy*
  • Neoplasms / enzymology*
  • Neoplasms / etiology
  • Phosphoinositide-3 Kinase Inhibitors
  • Phosphotransferases / physiology*
  • Piperazines
  • Protein Kinase Inhibitors*
  • Protein-Tyrosine Kinases / antagonists & inhibitors
  • Proto-Oncogene Proteins B-raf / genetics
  • Pyrimidines
  • Rituximab
  • Signal Transduction

Substances

  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Humanized
  • Antibodies, Monoclonal, Murine-Derived
  • Benzamides
  • Biomarkers, Tumor
  • Phosphoinositide-3 Kinase Inhibitors
  • Piperazines
  • Protein Kinase Inhibitors
  • Pyrimidines
  • Bevacizumab
  • Rituximab
  • Imatinib Mesylate
  • Phosphotransferases
  • ErbB Receptors
  • Protein-Tyrosine Kinases
  • Fusion Proteins, bcr-abl
  • Proto-Oncogene Proteins B-raf