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

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Abstract
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. Copyright © 2001 John Wiley & Sons, Ltd.

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