β-catenin nuclear expression correlates with cyclin D1 overexpression in sporadic desmoid tumours

The immunohistochemical expression of beta -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 beta -catenin within the nuclei could affect the regulation of the cyclin DI gene. There was a statistically significant correlation between beta -catenin accumulation and cyclin D1 overexpression (p = 0.029). Each group with beta -catenin accumulation or cyclin D1 overexpression showed a higher PCNA-LI than those wi 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 beta -catenin gene. Amplification of the cyclin DI 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 beta -catenin mutation fell within a wide range, from codon 21 to codon 67. In conclusion, beta -catenin nuclear expression correlated with cyclin D1 overexpression in sporadic desmoid tumours, which could be an in vivo model system for the APC-beta -catenin-Tcf pathway. In addition, beta -catenin mutations in desmoid tumours occurred at an unusually wide range of sites within the gene. Copyright (C) 2001 John Wiley & Sons, Ltd.