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Wnt pathway may not be implicated in all routes to colorectal cancer
  1. J R Jass
  1. Correspondence to:
    J R Jass
    Department of Pathology, McGill University, 3775 University Street, Montreal, Quebec, Canada H3A 2B4;jeremy.jass{at}mcgill.ca

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Schneikert and Behrens (Gut Published Online First: 13 July 2006. doi: 10.1136/gut.2006.093310) have produced a comprehensive and instructive overview of the Wnt signalling pathway and its role in colorectal tumorigenesis. They have emphasised that dysregulation of the Wnt pathway is a prerequisite for the initiation of colorectal neoplasia, and is also sufficient for explaining the early growth of neoplasms. They also state that aberrant activation of the Wnt signalling pathway occurs almost exclusively through the mutation of the two key regulators: adenomatous polyposis coli (APC) and β-catenin. However, if these premises are to be accepted, then it should be possible to show the mutation of either APC or β-catenin in virtually all primary colorectal cancers. Standard texts indeed state that approximately 80% of colorectal cancers (CRCs) have APC mutations and that β-catenin mutations occur in around 50% of the remaining CRCs.1 Similarly, Schneikert and Behrens suggest that up to 80% of CRCs have APC mutations, whereas 10% of CRCs have β-catenin mutation (sources not given).

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