Abstract
We investigated in the rat the role of the Apc gene, which is mutated in familial adenomatous polyposis and sporadic colon cancer in the process leading from normal colonic mucosa to aberrant crypt foci (ACF) and finally to adenomas and adenocarcinomas. We analysed mutations in exon 15 of the rat Apc gene using in vitro synthesized protein assay in 66 ACF and in 28 colon tumours induced by azoxymethane. No Apc mutations were found in ACF, whereas five mutations were found in the tumours. The data suggest that mutations of the Apc gene are associated with the transition from ACF to adenoma and adenocarcinoma and not from normal mucosa to ACF.
Highlights
Summary We investigated in the rat the role of the Apc gene, which is mutated in familial adenomatous polyposis and sporadic colon cancer in the process leading from normal colonic mucosa to aberrant crypt foci (ACF) and to adenomas and adenocarcinomas
We analysed mutations in exon 15 of the rat Apc gene using in vitro synthesized protein assay in 66 ACF and in 28 colon tumours induced by azoxymethane
No Apc mutations were found in ACF, whereas five mutations were found in the tumours
Summary
Induction and identification of ACF and colonic tumours. Male F344 rats (Nossan, Correzzana, Italy) were treated twice subcutaneously, 1 week apart, with 15 mg kg-' AOM and sacrificed between day 230 and day 245 after treatment. The colon was washed with saline, opened longitudinally and observed without formalin fixation under the microscope (40x magnification) to identify ACF according to Bird (1987). ACF were dissected under a stereomicroscope and stored at - 80°C to be tested for Apc mutations. Serial sections of a few dissected ACF showed that no more than 50% of a sample was made up of microscopically
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