Prognostic value of the preserved expression of the E-cadherin and catenin families of adhesion molecules and of β-catenin mutations in synovial sarcoma

This study addresses the immunohistochemical expression of the E-cadherin and catenin families and mutations of the β-catenin gene detected by PCR-SSCP in synovial sarcoma. Immunohistochemical analysis was performed for 72 cases, with follow-up data available on 62. The prognostic value of the expression of these proteins was evaluated. Reduced immunoreactivity for E-cadherin and α-catenin was significantly correlated with a poor survival rate (p = 0.0040 and 0.0053, respectively). According to multivariate analysis, low AJC stage (stages I and II: p< 0.0001), the preservation of α-catenin expression (p = 0.0001), and a low necrotic rate (< 50%: p = 0.0139) were independent favourable prognostic factors. Widespread aberrant staining of β-catenin protein within cytoplasm and/or nuclei was observed in 28 cases (38.9%) and was significantly correlated with poor survival (p = 0.0122). In addition, there was a trend towards a correlation between widespread aberrant staining of β-catenin and the MIB-1 labelling index (p = 0.0535). Mutational analysis of exon 3 of the β-catenin gene was performed for 49 cases. Nucleotide sequencing analysis revealed that four (8.2%) contained point mutations (three in codon 32, GAC to TAC; one in codon 37, TCT to TTT). Survival data were available for three out of four cases with β-catenin mutations; two of these patients died within 1 year (died of disease at 6 and 11 months, respectively). These results suggest that E-cadherin and α-catenin undertake important roles as intercellular adhesion molecules; their preserved expression is associated with a better overall survival rate in synovial sarcoma and may have prognostic value. Abnormal levels of β-catenin, with or without mutation, could contribute to the development and progression of synovial sarcoma, through increasing the proliferative activity of the tumour cells. Copyright (C) 2000 John Wiley and Sons, Ltd.