| First Author | Bjerknes M | Year | 1997 |
| Journal | Am J Pathol | Volume | 150 |
| Issue | 3 | Pages | 833-9 |
| PubMed ID | 9060821 | Mgi Jnum | J:38930 |
| Mgi Id | MGI:86316 | Citation | Bjerknes M, et al. (1997) APC mutation and the crypt cycle in murine and human intestine. Am J Pathol 150(3):833-9 |
| abstractText | 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 no normal APC +/- (ie, 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. |
