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PMID:9060821
| Citation |
Bjerknes, M, Cheng, H, Hay, K and Gallinger, S (1997) APC mutation and the crypt cycle in murine and human intestine. Am. J. Pathol. 150:833-9 |
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| 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. |
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| Keywords |
Adenomatous Polyposis Coli/genetics; Adenomatous Polyposis Coli/pathology; Aging/pathology; Animals; Colon/growth & development; Colon/pathology; Colonic Diseases/genetics; Colonic Diseases/pathology; Colonic Neoplasms/genetics; Colonic Neoplasms/pathology; Female; Genes, APC/genetics; Humans; Jejunum/pathology; Male; Mice; Mice, Inbred C57BL; Mutation; Precancerous Conditions/genetics; Precancerous Conditions/pathology; Species Specificity |
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Significance
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| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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