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Absent p53 Immunohistochemical Staining in a Pituitary Carcinoma

Published online by Cambridge University Press:  24 February 2017

Krishna Kumar ,
Robert J.B. Macaulay ,
Michael Kelly  and
Tyler Pirlot
Krishna Kumar*
Affiliation:
Department of Surgery, Section of Neurosurgery, Regina General Hospital, University of Saskatchewan, Regina, Saskatchewan
Robert J.B. Macaulay
Affiliation:
Department of Pathology and Laboratory medicine, Queen Elizabeth II Health Science Centre, Dalhousie University, Halifax, Nova Scotia, Canada
Michael Kelly
Affiliation:
Department of Pathology and Laboratory medicine, Queen Elizabeth II Health Science Centre, Dalhousie University, Halifax, Nova Scotia, Canada
Tyler Pirlot
Affiliation:
Department of Pathology and Laboratory medicine, Queen Elizabeth II Health Science Centre, Dalhousie University, Halifax, Nova Scotia, Canada
*
Suite 121, Medical Office Building, Regina General Hospital, 1440 14th Avenue, Regina, Saskatchewan, Canada, S4P 0W5
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Abstract:

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Background:

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.

Methods:

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.

Results:

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.

Conclusions:

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.

Résumé:

RÉSUMÉ:Introduction:

La transformation carcinomateuse d'un adénome pituitaire est rare et elle est généralement accompagnée par une accumulation nucléaire de la protéine p53. Le carcinome pituitaire sans accumulation de protéine p53 est très rare, seulement deux cas ayant été rapportés à date.

Méthodes:

On a découvert une masse suprasellaire chez un patient ayant consulté pour des troubles visuels accompagnés d'anomalies des nerfs crâniens. Il a subi une excision par voie transphénoïdale et par voie transfrontale d'un adénome pituitaire non fonctionnel qui a récidivé à plusieurs reprises. La troisième récidive s'est accompagnée de métastases durales multiples. Il a continué à développer des lésions intracrâniennes additionnelles malgré un traitement chirurgical agressif. Le patient est décédé deux ans après la découverte des premières métastases. Des spécimens anatomopathologiques de 1984, 1995, 1997 et 1998 étaient disponibles pour analyse histologique et immunocytochimique. Des anticorps reconnaissant les hormones pituitaires (ACTH, PRL, GH, FSH, LH et TSH), ainsi que la cytokératine, l'antigène de la membrane épithéliale (EMA), la protéine gliofibrillaire acide (GFAP) et la chromogranine A ont été appliqués pour déterminer l'origine du cancer. Un antisérum spécifique pour le Ki-67 (MIB-1) et la protéine p53 ont également été appliqués pour mieux définir la biologie de la tumeur.

Résultats:

Bien qu'on ait détecté de la cytokératine et de la chromogranine A dans les cellules néoplasiques, aucune expression d'hormones pituitaires n'a été observée, ce qui indique qu'il s'agissait d'un adénome pituitaire non fonctionnel à cellules nulles. Le pléomorphisme nucléaire et l'activité mitotique ont augmenté d'une résection à l'autre. Une accumulation anormale de la protéine p53 n'a pas été observée, que ce soit dans les premières résections ou dans le tissu métastatique.

Conclusions:

Le fait de ne pas observer d'accumulation de la protéine p53 ne garantit pas un bon pronostic chez les cas d'adénomes pituitaires. Il peut s'agir d'un carcinome pituitaire, même s'il n'y a pas d'accumulation de la protéine p53. Les facteurs sous-jacents au comportement agressif des néoplasies pituitaires sont mal connus et demeurent à l'étude.

Type
Case Report
Information
Canadian Journal of Neurological Sciences , Volume 28 , Issue 2 , May 2001 , pp. 174 - 178
Copyright
Copyright © The Canadian Journal of Neurological 2000

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