BCL-2, P53 AND MIB-1 EXPRESSION IN NORMAL AND NEOPLASTIC PARATHYROID TISSUES

An altered control of the mechanisms involved in cell proliferation an d programmed cell death (apoptosis) might play an important role in pa rathyroid tumorigenesis. We evaluated by immunohistochemistry the expr ession of bcl-2 and p53 proteins, as markers of apoptosis control, and MIB-1, as marker of cell proliferation, in a series of normal and neo plastic parathyroid tissues. The specimens were 33 normal parathyroids , 43 parathyroid adenomas and 3 parathyroid carcinomas. Results were s cored as positive when more than 1% of cells were stained for MIB-1 an d p53, and more than 10% for bcl-2. All normal parathyroids showed num erous bcl-2 positive cells (greater than or equal to 80%), low prolife ration rate (MIB-1) and no p53 protein expression. Twenty-four (55%) a denomas were bcl-2 positive; in 16 of these the number of positive cel ls was high (>50%) and immunoreactivity was diffusely distributed with in the adenoma; 8 cases showed a zonal staining pattern, in which grou ps of stained cells were surrounded by negative cells. Nineteen adenom as (45%) and all carcinomas were bet-2 negative. A high proliferative rate (MIB-1) was found in all carcinomas and 4 adenomas (9%); all MIB- 1 positive adenomas were bcl-2 negative. p53 was negative in all speci mens. No significant differences in serum calcium and intact PTH level s nor in tumor size were found between bcl-2 negative and bcl-2-positi ve and MIB-1-positive and MIB-1-negative adenomas. An inverse, but not statistically significant (p=0.06) correlation was observed between t he percentage of bcl-2 positive cells and serum calcium level in parat hyroid adenomas. In conclusion, parathyroid adenomas are a heterogeneo us group of lesions in which the pattern of bcl-2 and MIB-1 protein ex pression ranges between that of normal parathyroid (bcl-2 positivity a nd MIB-1 negativity) and that of parathyroid carcinoma (bcl-2 negativi ty and MIB-1 positivity). The question of whether the finding of the M IB-1 positive-bcl-2 negative phenotype identifies a subgroup of clinic ally more aggressive adenomas remains to be established. (C) 1998, Edi trice Kurtis.