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

Anna Pavlina G Haramis, Adam Hurlstone, Yme van der Velden, Harry Begthel, Maaike van den Born, G. Johan A Offerhaus, Hans C. Clevers

Research output: Contribution to journalArticlepeer-review

Abstract

Truncation of the tumour suppressor adenomatous polyposis coli (APC) constitutively activates the Wnt/β-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 β-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 (US)
Pages (from-to)444-449
Number of pages6
JournalEMBO Reports
Volume7
Issue number4
DOIs
StatePublished - Apr 2006
Externally publishedYes

Keywords

  • APC
  • Cancer
  • Zebrafish

ASJC Scopus subject areas

  • Genetics
  • Cell Biology

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