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Carcinomatous transformation of pituitary adenomas is uncommon, and is generally accompanied by nuclear accumulation of p53 protein. Pituitary carcinoma lacking accumulation of p53 protein is very rare, only two such cases being previously reported.
A patient presented with visual disturbance and cranial nerve palsies and was found to have a suprasellar mass. He underwent both transphenoidal and transfrontal excision of a nonfunctioning pituitary adenoma which recurred several times. The third recurrence was accompanied by multiple dural-based metastases. Despite aggressive surgical management, he continued to develop additional intracranial lesions and died two years after the discovery of metastatic disease. Specimens from 1984, 1995, 1997 and 1998 were available for histological and immunocytochemical analysis. Antibodies recognizing the pituitary hormones (ACTH, PRL, GH, FSH, LH and TSH), as well as cytokeratin, epithelial membrane antigen (EMA), glial fibrillary acidic protein (GFAP) and chromogranin A were applied to investigate the lineage of the neoplasm. Antisera specific for Ki-67 (MIB-1) and p53 protein were also applied to further delineate the biology of the tumour.
Although cytokeratin and chromogranin A were detected in neoplastic cells, no expression of pituitary hormones was demonstrable, indicative of a nonfunctioning, null-cell pituitary adenoma. Nuclear pleomorphism and mitotic activity increased with subsequent resections. Abnormal accumulation of p53 protein was not observed, neither in early resections nor in the metastatic deposits.
Failure to demonstrate p53 protein accumulation does not ensure a favourable outcome for pituitary adenoma. Accordingly, pituitary carcinoma may occur in the absence of p53 accumulation. The factors which underlie aggressive behaviour of pituitary neoplasms are uncertain but are under investigation.
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