P53 TUMOR-SUPPRESSOR GENE-EXPRESSION IN HYPERPARATHYROIDISM

Background: Mutations of the p53 tumour suppressor gene lead to the lo ss of control of normal cellular proliferation and differentiation and have been shown to be associated with the development of malignancy. Method: Archival paraffin resection specimens from 86 cases of hyperpa rathyroidism treated surgically using the rabbit poly clonal CMI antib ody were investigated to detect p53 immunoreactivity in these sections . Results: Eighteen of the 86 sections examined (21%) showed nuclear i mmunoreactivity. No correlation was detected between tumour histology and p53 immunoreactivity (P = 0.45), nor was there any correlation bet ween tumour clonality and immunoreactivity (P = 0.54). Multiple endocr ine neoplasia type 1 (MEN 1) status did not correlate with p53 immunor eactivity, A significant correlation between p53 immunoreactivity and preparathyroidectomy calcium levels of > 1.5 mmol/L was detected (P < 0.005) although no correlation was noted between p53 immunoreactivity and higher levels of preparathyroidectomy intact parathyroid hormone ( PTH) levels. Conclusion: A relationship is postulated between abnormal serum calcium regulation and p53 mutation in hypercalcaemic stales as sociated with hyperparathyroidism.