APC, beta-Catenin and hTCF-4; an unholy trinity in the genesis of colorectal cancer

Eur J Surg Oncol. 2003 Mar;29(2):107-17. doi: 10.1053/ejso.2002.1331.


Mutations in APC have been identified in up to 80% of 'classic' sporadic colorectal cancers. Although the APC gene was first sequenced over a decade ago, new functions are still being described and its importance in the genesis of colorectal cancer continues to increase. The current focus of attention is on the APC/beta-Catenin/TCF signal transduction pathway as the main effector mechanism, and recent work has also implicated this pathway in the aetiology of the minority of CRCs that develop through mismatch repair. At the same time, new evidence on the interactions of APC with the cytoskeleton and the demonstration of a nuclear export function in the protein have shown that it has multiple additional roles in colorectal carcinogenesis. Thus this is an area that benefits from further review of the ever expanding literature.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adenomatous Polyposis Coli / genetics
  • Adenomatous Polyposis Coli / physiopathology
  • Cadherins / genetics*
  • Cadherins / physiology
  • Cell Adhesion / physiology
  • Cell Movement / physiology
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms / physiopathology
  • Cytoskeletal Proteins / genetics*
  • Cytoskeletal Proteins / physiology
  • Genes, APC / physiology*
  • Humans
  • Mutation
  • Signal Transduction
  • TCF Transcription Factors
  • Trans-Activators / genetics*
  • Trans-Activators / physiology
  • Transcription Factor 7-Like 2 Protein
  • Transcription Factors / genetics*
  • Transcription Factors / physiology
  • beta Catenin


  • CTNNB1 protein, human
  • Cadherins
  • Cytoskeletal Proteins
  • TCF Transcription Factors
  • TCF7L2 protein, human
  • Trans-Activators
  • Transcription Factor 7-Like 2 Protein
  • Transcription Factors
  • beta Catenin