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

A.-P.G. Haramis, A. Hurlstone, Y. van der Velden, H. Begthel, M. van den Born, G.J.A. Offerhaus, J.C. Clevers

Research output: Contribution to journal/periodicalArticleScientificpeer-review

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.
Original languageEnglish
Pages (from-to)444-449
JournalEMBO Reports
Volume7
Publication statusPublished - 2006

Fingerprint Dive into the research topics of 'Adenomatous polyposis coli-deficient zebrafish are susceptible to digestive tract neoplasia.'. Together they form a unique fingerprint.

  • Cite this

    Haramis, A-PG., Hurlstone, A., Velden, Y. V. D., Begthel, H., Born, M. V. D., Offerhaus, G. J. A., & Clevers, J. C. (2006). Adenomatous polyposis coli-deficient zebrafish are susceptible to digestive tract neoplasia. EMBO Reports, 7, 444-449.