A mouse model of human familial adenomatous polyposis
โ Scribed by Yang, Kan; Edelmann, Winfried; Fan, Kunhua; Lau, Kirkland; Kolli, Venkateswara R.; Fodde, Riccardo; Khan, P. Meera; Kucherlapati, Raju; Lipkin, Martin
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 248 KB
- Volume
- 277
- Category
- Article
- ISSN
- 0022-104X
No coin nor oath required. For personal study only.
โฆ Synopsis
In an effort to generate a good mouse model for human colorectal cancer, we generated mice which carry a mutation in the adenomatous polyposis coli (Apc) gene. Mice which are heterozygous for the mutation, designated Apc1638, develop colonic polyps and tumors of the small intestine. Neoplasms were found in 96% of animals studied, and they included adenomas, adenocarcinomas, and polypoid hyperplasias. The mice developed an average of 3.3 tumors, with the highest number in duodenum, followed by jejunum, stomach, ileum, and colon. Focal areas of dysplasias were observed in the colonic mucosa in 50% of mice which were 10 months old or older. These results suggest that mice carrying the Apc1638 mutation can serve as a good model to study the initiation, progression, and inhibition of gastrointestinal tumors.
๐ SIMILAR VOLUMES
Familial adenomatous polyposis (FAP) is characterized by the presence of more than 100 colorectal adenomatous polyps with an almost inevitable progression to cancer. At-risk individuals are screened and, if affected, prophylactic colectomy is performed. Operative options include total colectomy with