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Departments of Pathology [W. S. S.] and Oncological Sciences [M. D. P., M. L. S.], University of Utah Health Sciences Center, Salt Lake City, Utah 84132; The Whitehead Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142 [L. N. S.]; V.I.B. Department of Molecular Biology, Molecular Cell Biology Unit, University of Ghent, B-9000 Ghent, Belgium [F. N., F. v. R.]
Loss of serine or threonine phosphorylation sites from exon 3 of ß-catenin has been identified in approximately half of colorectal tumors which lack adenomatous polyposis coli (APC) mutations, but the overall contribution of ß-catenin mutations to sporadic colorectal tumorigenesis is unclear. We therefore used PCR to amplify and sequence exon 3 of ß-catenin from 202 sporadic colorectal tumors. Exon 3 ß-catenin mutations were identified in 6 of 48 small (<1 cm) adenomas, 2 of 82 large (
1 cm) adenomas, and 1 of 72 invasive carcinomas. Eight of the nine mutations, including all of those in the small adenomas and the invasive cancer, involved loss of serine or threonine phosphorylation sites. The percentage of ß-catenin mutations in small adenomas (12.5%) was significantly greater than that in large adenomas (2.4%) and invasive cancers (1.4%; P = 0.05 and P = 0.02, respectively). We conclude that mutation of ß-catenin can be an early, perhaps initiating, event in colorectal tumorigenesis. Small adenomas with ß-catenin mutations do not appear to be as likely to progress to larger adenomas and invasive carcinomas as other adenomas, however, with the result that ß-catenin mutations are only rarely seen in invasive cancers. This suggests that APC and ß-catenin mutations are not functionally equivalent, and that the APC gene may have other tumor suppressor functions besides the degradation of ß-catenin.
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