The many ways of Wnt in cancer

Curr Opin Genet Dev. 2007 Feb;17(1):45-51. doi: 10.1016/j.gde.2006.12.007.


More than 20 years ago, the oncogenicity of a Wnt ligand was revealed in a series of experiments originating with random proviral integration in mice. The significance of Wnt signaling in human cancer has since been buttressed by the identification of mutations in genes coding for the Wnt pathway components Axin, APC, and beta-catenin. This review summarizes the reported genetic defects in the Wnt pathway, with an emphasis on their functional contribution to human tumor progression.

Publication types

  • Review

MeSH terms

  • Axin Protein
  • Genes, APC*
  • Glycogen Synthase Kinase 3 / genetics
  • Humans
  • Intracellular Signaling Peptides and Proteins
  • Models, Biological
  • Mutation / genetics*
  • Neoplasms / genetics*
  • Proteins / genetics
  • Repressor Proteins / genetics*
  • Signal Transduction / genetics*
  • TCF Transcription Factors / genetics
  • Transcription Factor 7-Like 2 Protein
  • Wnt Proteins / genetics*
  • beta Catenin / genetics*


  • Axin Protein
  • Intracellular Signaling Peptides and Proteins
  • Proteins
  • Repressor Proteins
  • TCF Transcription Factors
  • TCF7L2 protein, human
  • Tcf7l2 protein, mouse
  • Transcription Factor 7-Like 2 Protein
  • WD repeat containing planar cell polarity effector
  • Wnt Proteins
  • beta Catenin
  • Glycogen Synthase Kinase 3