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Adenomatous polyposis coli-deficient zebrafish are susceptible to digestive tract neoplasia.

Haramis, A.-P.G. and Hurlstone, A. and Velden, Y. van der and Begthel, H. and Born, M. van den and Offerhaus, G.J.A. and Clevers, J.C. (2006) Adenomatous polyposis coli-deficient zebrafish are susceptible to digestive tract neoplasia. EMBO reports, 7(4), 444-449. ISSN 1469221X. doi: 10.1038/sj.embor.7400638. PMC_URL: http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=1456916&blobtype=pdf.

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Abstract

Truncation of the tumour suppressor adenomatous polyposis coli (APC) constitutively activates the Wnt/beta-catenin signalling pathway. This event constitutes the primary transforming event in sporadic colorectal cancer in humans. Moreover, humans or mice carrying germline truncating mutations in APC develop large numbers of intestinal adenomas. Here, we report that zebrafish that are heterozygous for a truncating APC mutation spontaneously develop intestinal, hepatic and pancreatic neoplasias that are highly proliferative, accumulate beta-catenin and express Wnt target genes. Treatment with the chemical carcinogen 7,12-dimethylbenz[a]anthracene accelerates the induction of these lesions. These observations establish apc-mutant zebrafish as a bona fide model for the study of digestive tract cancer.

Item Type:Article
Additional Information:doi: 10.1038/sj.embor.7400638. PMC_URL: http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=1456916&blobtype=pdf
Institutes:Hubrecht Instituut
ID Code:3597
Deposited On:13 Feb 2009 17:14
Last Modified:10 Dec 2009 13:14

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