[The role of APC in colonic cancerogenesis: zeroing in on Myc]

Bull Cancer. 1998 Nov;85(11):925-8.
[Article in French]


The APC gene is mutated both in familial adenomatous polyposis (FAP) and sporadic colorectal cancers. It had been previously shown that the APC gene product interacts with beta-catenin, a key element in the Wnt-1 signaling pathway. This pathway is initiated by the growth factor Wnt-1 and ends up in the nucleus where it activates transcription factors of the Lef/Tcf family although the targets of the latter were still unknown. This has just been accomplished by the identification of the c-MYC oncogene as the relevant target of the Wnt-1/APC pathway in the development of human colorectal cancers. Indeed, under appropriate conditions (presence of growth factors, for example), c-MYC is an essential determinant of cell proliferation.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Adenomatous Polyposis Coli / genetics
  • Adenomatous Polyposis Coli Protein
  • Cytoskeletal Proteins / metabolism*
  • Genes, APC / genetics*
  • Genes, APC / physiology
  • Genes, myc / genetics*
  • Genes, myc / physiology
  • Humans
  • Mammary Tumor Virus, Mouse / genetics
  • Proto-Oncogene Proteins / metabolism*
  • Signal Transduction
  • Trans-Activators*
  • Wnt Proteins
  • Wnt1 Protein
  • Zebrafish Proteins*
  • beta Catenin


  • Adenomatous Polyposis Coli Protein
  • CTNNB1 protein, human
  • Cytoskeletal Proteins
  • Proto-Oncogene Proteins
  • Trans-Activators
  • WNT1 protein, human
  • Wnt Proteins
  • Wnt1 Protein
  • Zebrafish Proteins
  • beta Catenin