The oncogenic activation of beta-catenin

Curr Opin Genet Dev. 1999 Feb;9(1):15-21. doi: 10.1016/s0959-437x(99)80003-3.


The activation of beta-catenin to an oncogenic state can result from the inactivation of the tumor suppressor adenomatous polyposis coli (APC), by direct mutation in the beta-catenin gene, or by the activation of wnt receptors. Once activated, beta-catenin most likely promotes tumor progression through its persistent interaction with one or more of its numerous downstream targets.

Publication types

  • Review

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Cytoskeletal Proteins / genetics*
  • Gene Expression Regulation
  • Genes, APC
  • Humans
  • Mutation
  • Neoplasms / genetics*
  • Oncogenes / genetics
  • Proto-Oncogene Proteins
  • Trans-Activators*
  • Wnt Proteins
  • Zebrafish Proteins*
  • beta Catenin


  • CTNNB1 protein, human
  • Cytoskeletal Proteins
  • Proto-Oncogene Proteins
  • Trans-Activators
  • Wnt Proteins
  • Zebrafish Proteins
  • beta Catenin