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Publication : Genotype-phenotype correlation in murine Apc mutation: differences in enterocyte migration and response to sulindac.

First Author  Mahmoud NN Year  1999
Journal  Cancer Res Volume  59
Issue  2 Pages  353-9
PubMed ID  9927046 Mgi Jnum  J:52043
Mgi Id  MGI:1327734 Citation  Mahmoud NN, et al. (1999) Genotype-phenotype correlation in murine Apc mutation: differences in enterocyte migration and response to sulindac. Cancer Res 59(2):353-9
abstractText  The adenomatous polyposis coli (APC) gene product mediates coordinated cell growth in the intestinal mucosa, In humans, germ-line mutations of APC are associated with colorectal carcinogenesis, a process that varies in severity depending on the length of the protein resulting from the mutant allele. In a previous study of the C57BL/ 6J-Min/+ (Min/+) mouse, we found that the protein fragment resulting from truncation at codon 850 of murine Ape was associated with changes in enterocyte migration, proliferation, apoptosis, and beta-catenin expression. This effect was reversed upon treatment of Min/+ mice with, the chemopreventive drug sulindac sulfide. In this study, we measured enterocyte migration in the Apc1638N mouse, an animal with an Ape mutation that yields no detectable APC protein. We found no difference in enterocyte migration, proliferation, apoptosis, or beta- catenin levels in the Ape1638N mouse when compared to wild- type littermates bearing two normal Ape alleles, Furthermore, administration of sulindac sulfide to Apc1638N mice did not alter enterocyte migration. These observations suggest that a dominant negative effect altering cell migration is exerted by the truncated APC protein present in the Min/+ mouse. These data also suggest that the effectiveness of chemopreventive agents in preventing Ape-related tumor formation may depend on which type of mutation is present.
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