P. Subramaniam et al., INACTIVATION OF RETINOBLASTOMA GENE IN MALIGNANT PARATHYROID GROWTHS - A CANDIDATE GENETIC TRIGGER, Australian and New Zealand journal of surgery, 65(10), 1995, pp. 714-716
The molecular basis for parathyroid carcinoma remains undetermined. Pa
rathyroid carcinoma potentially remains curable by early en bloc resec
tion. This requires a reliable diagnostic tool as histological feature
s alone are insufficient to distinguish parathyroid carcinoma from its
benign counterpart, parathyroid adenoma. A variety of human cancers a
rise from the inactivation of the retinoblastoma (RE) gene, a tumour-s
uppressor gene on chromosome 13q14. We investigated the role of this g
ene in parathyroid growths by using a mouse monoclonal antibody to det
ect RE gene expression immunohistochemically. Two of the three parathy
roid carcinomas in this study showed evidence of RE gene inactivation
compared with one of 11 benign parathyroid entities. Three normal para
thyroid glands stained showed strong evidence of RE gene expression in
all three glands. The relationship between RE gene inactivation and p
arathyroid malignancy, however, was not statistically significant.