The role of the Wnt signalling pathway in colorectal tumorigenesis.
Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes. Mutations in the tumour suppressor APC (adenomatous polyposis coli) genes occur early in the development of CRC and lead to the stabilization of the Wnt pathway component beta-catenin and to the constitutive activation of Wnt signalling. Stabilizing mutations of beta-catenin can also lead to its accumulation, qualifying beta-catenin as a proto-oncogene. Here I will summarize the biochemical interactions occurring in Wnt signalling and describe how alterations in Wnt pathway components lead to CRC.
Behrens
J
J
Nikolaus-Fiebiger-Center for Molecular Medicine, University Erlangen-Nürnberg, Glueckstr. 6, D-91054 Erlangen, Germany. jbehrens@molmed.uni-erlangen.de
D015179:Colorectal Neoplasms / Q000235:genetics*; D017491:Genes, APC; D006801:Humans; D009154:Mutation; D011505:Protein-Tyrosine Kinases / Q000235:genetics; D000090063:Proto-Oncogene Mas; D015398:Signal Transduction / Q000235:genetics
C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; D011505:Protein-Tyrosine Kinases