The stem cell factor receptor/c-Kit as a drug target in cancer

Curr Cancer Drug Targets. 2006 Feb;6(1):65-75. doi: 10.2174/156800906775471725.

Abstract

Tyrosine phosphorylation has a key role in intracellular signaling. Inappropriate proliferation and survival cues in tumor cells often occur as a consequence of unregulated tyrosine kinase activity. Much of the current development of anti-cancer therapies tries to target causative proteins in a specific manner to minimize side-effects. One attractive group of target proteins is the kinases. c-Kit is a receptor tyrosine kinase that normally controls the function of primitive hematopoietic cells, melanocytes and germ cells. It has become clear that uncontrolled activity of c-Kit contributes to formation of an array of human tumors. The unregulated activity of c-Kit may be due to overexpression, autocrine loops or mutational activation. This makes c-Kit an excellent target for cancer therapies in these tumors. In this review we will highlight the current knowledge on the signal transduction molecules and pathways activated by c-Kit under normal conditions and in cancer cells, and the role of aberrant c-Kit signaling in cancer progression. Recent advances in the development of specific inhibitors interfering with these signal transduction pathways will be discussed.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology*
  • Humans
  • Neoplasms / drug therapy*
  • Neoplasms / genetics
  • Proto-Oncogene Proteins c-kit / drug effects*
  • Signal Transduction / drug effects

Substances

  • Antineoplastic Agents
  • Proto-Oncogene Proteins c-kit