The immunohistochemical expression of β-catenin, cyclin D1, Ki-67 and PCNA was Examined in 38 cases of sporadic extra-abdominal or abdominal-wall desmoid tumours without familial adenomatous polyposis (FAP), to evaluate the hypothesis that the accumulated β-catenin within the nuclei could affect the regulation of the cyclin D1 gene. There was a statistically significant correlation between β-catenin accumulation and cyclin D1 overexpression (p=0.029). Each group with β-catenin accumulation or cyclin D1 overexpression showed a higher PCNA-LI than those without, the difference being statistically significant (p=0.007, p=0.004, respectively). Differential PCR was also performed to detect amplification of the cyclin D1 gene and mutational analysis was undertaken for exon 3 of the β-catenin gene. Amplification of the cyclin D1 gene was observed in 13 out of 22 cases (59.1%). There were nine-point mutations in 7 out of 18 cases (38.9%). The distribution of β-catenin mutation fell within a wide range, from codon 21 to codon 67. In conclusion, β-catenin nuclear expression correlated with cyclin D1 overexpression in sporadic desmoid tumours, which could be an in vivo model system for the APC-β-catenin-Tcf pathway. In addition, β-catenin mutations in desmoid tumours occurred at an unusually wide range of sites within the gene.
All Science Journal Classification (ASJC) codes
- Pathology and Forensic Medicine