Carcinogen-induced pancreatic lesions in the mouse: effect of Smad4 and Apc genotypes

Cullingworth, Jan, Hooper, Martin L., Harrison, David J., Mason, John O., Sirard, Christian, Patek, Charles E. and Clarke, Alan Richard ORCID: https://orcid.org/0000-0002-4281-426X 2002. Carcinogen-induced pancreatic lesions in the mouse: effect of Smad4 and Apc genotypes. Oncogene 21 (30) , pp. 4696-4701. 10.1038/sj.onc.1205673

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Abstract

Mutations in the tumour suppressor genes SMAD4 (DPC4, deleted in pancreatic cancer locus 4) and adenomatous polyposis coli (APC) have been implicated in the development of pancreatic cancer in humans. Treatment of wild-type, Smad4+/-, ApcMin/+ or ApcMin/+Smad4+/- mice with N-Nitroso-N-Methyl Urea (NMU) results in abnormal foci in pancreatic acinar cells characterized by increased levels of -catenin. Previously such foci have been shown to be the precursors of pancreatic neoplasia. Interestingly, only NMU-treated ApcMin/+Smad4+/- mice exhibit a significant increase in abnormal pancreas, which was found to be due to increased number of abnormal foci rather than increased focus size. A range of foci sizes were analysed, but only smaller abnormal foci were characterized by morphological nuclear atypia. These studies suggest functional co-operation between TGF- and Wnt signalling pathways in the suppression of pancreatic tumorigenesis in the mouse.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences European Cancer Stem Cell Research Institute (ECSCRI)
Subjects:	Q Science > Q Science (General) Q Science > QH Natural history > QH426 Genetics
Uncontrolled Keywords:	Pancreas; SMAD4; APC; mouse.
Publisher:	Nature Publishing
ISSN:	0950-9232
Last Modified:	25 Oct 2022 10:11
URI:	https://orca.cardiff.ac.uk/id/eprint/61375

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