bc1 - 2 Expresseion in Malignant Melanoma and Melanocytic Nevus / 대한피부과학회지

ABSTRACT

BACKGROUND: The bcl-2 is a newly known oncogene involved in tumorigenisis by blocking apoptosis or programmed cell death. Overexpression of bcl-2 protein has been detected in a variety of human malignancies. However, recent studies of the expression of bcl-2 protein in human melanoma and melanocytic nevus have been controversial. OBJECTIVE: The purpose of this study was to examine whether there are any differences in the expression of bcl-2 protein between melanocytic nevus and rnalignant melanoma. METHODS: Immunohistochemical analysis of bcl-2 protein expression was performed on the formalin-fixed, paraffin-embedded tissue sections of 22 melanocytic nevus and 29 malignant melanomas (20 primary and 9 metastatic) using anti bcl-2 monoclonal antibody with an avidin-biotin peroxidase complex procedure. RESULTS: The results were as follows. 1. The positive rate for bcl-2 protein was observed in 95.4% (21/22) of melanocytic nevus and 95.0% (19/20) of primary malignant melanomas. Therefore, there was no significant difference between the two groups in the positive rate for bcl-2 prtoein. 2. The percentage of stained cells and the staining intensity of bcl-2 protein were significantly increased in melanocytic nevus compared to malignant melanoma (p<0.05). 3. The positive rate for bcl-2 expression of metastatic malignant melanoma [44.4% (4/9)] was significantly decreased compared to that of primary malignant melanoma [95.0%(19/20) ] (p<0. 05). But, there was no significant difference betweeen tumor thickness and histological type of malignant, melanoma in the expression of bcl-2 protein. 4. In melanocytic nevus, immunoreactivity of bcl-2 protein gradually diminished or even disappeared towards the deep dermis. CONCLUSION: the bcl-2 expression was decreased in malignant melanoma compared to melanocytic nevus. It. suggests that the loss of bcl-2 expression may play a significant role in the progression and metastasis of malignant melanoma.