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First published online March 4, 2005

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Where colorectal cancer starts

Mutations in the APC (adenomatous polyposis coli) gene occur in most sporadic colorectal cancers. But although APC loss is important in tumour initiation, it is unclear whether tumours form in the epithelial stem cells of the intestinal crypts or in the differentiated cells of the villus. On p. 1443, Andreu and colleagues report that Apc loss in the mouse intestine rapidly induces crypt-restricted premalignant changes. Using a conditional gene-ablation approach, they examined the effects of Apc loss along the crypt-villus axis of the mouse small intestine. Apc loss activates ß-catenin signalling in both compartments but only the crypt cells respond with increased proliferation and apoptosis, and impaired cell migration. The activation of ß-catenin signalling also alters crypt cell fate, promoting their commitment to the Paneth cell lineage. Overall, these results indicate that tumorigenesis caused by the loss of Apc in the colon occurs among the stem cells in the crypt base.

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Related articles in Development:

Crypt-restricted proliferation and commitment to the Paneth cell lineage following Apc loss in the mouse intestine

Pauline Andreu, Sabine Colnot, Cécile Godard, Sophie Gad, Philippe Chafey, Michiko Niwa-Kawakita, Pierre Laurent-Puig, Axel Kahn, Sylvie Robine, Christine Perret, and Béatrice Romagnolo
Development 2005 132: 1443-1451. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?