| Title | APC mutation and the crypt cycle in murine and human intestine. | | Author(s) | Bjerknes M, Cheng H, Hay K, Gallinger S | | Institution | Department of Anatomy and Cell Biology, University of Toronto, Ontario, Canada. | | Source | Am J Pathol 1997 Mar; 150(3):833-9. | | MeSH | Adenomatous Polyposis Coli
Aging
Animals
Colon
Colonic Diseases
Colonic Neoplasms
Female
Genes, APC
Humans
Jejunum
Male
Mice
Mice, Inbred C57BL
Mutation
Precancerous Conditions
Research Support, Non-U.S. Gov't
Species Specificity
| | Abstract | Dysplastic colon adenomas are thought to arise from growth of clones of APC -/- colonic epithelial cells. Isolated clusters of dysplastic crypts are often observed in patients with familial adenomatous polyposis. These patients have genotype APC +/-, and the clusters of dysplastic crypts (called microadenoma or aberrant crypt foci) are thought to represent an early stage in the expansion of a mutant clone of APC -/- cells. It is thought that the growth of these clusters of mutant crypts results from crypt replication through a process similar to what occurs in the normal crypt cycle. We measured the relative replication rate of mutant crypts by analyzing the size of clusters of mutant crypts in APC +/- individuals and found that mutant APC -/- crypts replicate more rapidly than do normal APC +/- (i.e., nonneoplastic) crypts. In contrast, the replication rate of mutant crypts in Apc +/- mice is not significantly different from that of normal crypts, thus supporting previous findings that aberrant crypt foci do not contribute significantly to the colon adenoma population in adult Apc +/- mice. Intriguingly, we found an effect of Apc heterozygosity on the frequency of branching crypts in young mice. | | Language | eng | | Pub Type(s) | Journal Article
| | PubMed ID | 9060821 |
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