Immunohistochemical analysis of the S100A1, S100B, CD44 and Bcl-2 antigens and the rate of cell proliferation assessed by Ki-67 antibody in benign and malignant melanocytic tumours

Abstract

Malignant melanomas usually have an unfavourable prognosis and poor response to chemotherapy. Deregulation of cell proliferation, programmed cell death and intercellular interactions are among several important mechanisms that might lead to malignant transformation of melanocytes and melanoma progression. The S100A1, S100B, Bcl-2 and CD44 antigens have all been described as being involved in different processes of melanoma progression. The expression of these antigens, as well as the rate of cell proliferation, was analyzed retrospectively in melanocytic tumours from 126 patients (32 males and 94 females, age ranging from 11 to 91 years). The series included benign (45 intradermal, 27 compound and eight displastic naevi) and malignant (39 primary and 14 metastatic) melanocytic tumours. The proliferating rate assessed by Ki-67 staining was lower in naevi than in melanomas, with a correlation coefficient of r = 0814. There was no overlap for rate of proliferation between benign and malignant tumours. The expression of S100A1 was low in benign melanocytic tumours and increased in malignant melanomas (r = 0.61). In contrast, a higher percentage of S100B antigen-positive cells were observed in benign melanocytic lesions than in melanomas (Pearson correlation coefficient, 0.627). In addition, positive immunostaining for S100B antigen in malignant melanomas corresponded with the areas with increased proliferating rate. The expression of Bcl-2 was lower in melanomas than in benign melanocytic tumours (r = -0.53). Bcl-2-negative areas within melanomas had an increased proliferating rate. The expression of CD44 showed a large variation both in benign and malignant melanocytic tumours. CD44 antigen expression was higher in melanomas with known metastases than in those without metastases, but this difference was not statistically significant.