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Immunohistochemical profile and chromosomal imbalances in papillary tumours of the pineal region
Author(s) -
Hasselblatt M.,
Blümcke I.,
Jeibmann A.,
Rickert C. H.,
Jouvet A.,
Van De Nes J. A. P.,
Kuchelmeister K.,
Brunn A.,
FevreMontange M.,
Paulus W.
Publication year - 2006
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.2006.00723.x
Subject(s) - choroid plexus , synaptophysin , glial fibrillary acidic protein , pathology , cytokeratin , immunohistochemistry , ependymoma , biology , staining , anatomy , medicine , endocrinology , central nervous system
The histopathology of papillary tumours of the pineal region (PTPR) closely resembles that of ependymomas and choroid plexus tumours. Therefore, immunohistochemical staining profiles were investigated in a series of 15 PTPR. In addition to cytokeratin, synaptophysin and glial fibrillary acidic protein expression, PTPR were examined for the presence of dot‐ or ring‐like epithelial membrane antigen (EMA) immunoreactivity typically encountered in ependymoma, staining for inwardly rectifying potassium channel Kir7.1 and stanniocalcin‐1 (specifically expressed in choroid plexus tumours) as well as microtubule‐associated protein‐2 (MAP‐2). Furthermore, comparative genomic hybridization was performed in five PTPR. Cytokeratin was expressed in all PTPR examined, whereas glial fibrillary acidic protein and synaptophysin staining were absent. Dot‐ or ring‐like EMA immunoreactivity was only observed in 1 out of 15 PTPR. Membranous Kir7.1 and cytoplasmic stanniocalcin‐1 staining were present in the minority of PTPR (3/15 and 4/15, respectively). In contrast, MAP‐2 immunoreactivity was encountered in 13 out of 15 PTPR, but was significantly less frequently observed in a series of choroid plexus tumours (7/37). PTPR mainly presented with chromosomal losses affecting chromosomes 10 (4/5 cases) and 22q (3/5 cases) as well as gains on chromosomes 4 (4/5 cases), 8 (3/5 cases), 9 (3/5 cases) and 12 (3/5 cases). To conclude, the majority of PTPR can be distinguished from ependymomas and choroid plexus tumours by absent staining for epithelial membrane antigen, Kir7.1 and staniocalcin‐1 as well as the presence of distinct MAP‐2 immunoreactivity. Antibodies directed against these antigens are thus expected to be valuable markers in the diagnosis of papillary tumours located in the vicinity of the third ventricle.