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Epithelial and pseudoepithelial differentiation in glioblastoma and gliosarcoma
A comparative morphologic and molecular genetic study
Article first published online: 24 SEP 2008
Copyright © 2008 American Cancer Society
Volume 113, Issue 10, pages 2779–2789, 15 November 2008
How to Cite
Rodriguez, F. J., Scheithauer, B. W., Giannini, C., Bryant, S. C. and Jenkins, R. B. (2008), Epithelial and pseudoepithelial differentiation in glioblastoma and gliosarcoma. Cancer, 113: 2779–2789. doi: 10.1002/cncr.23899
- Issue published online: 3 NOV 2008
- Article first published online: 24 SEP 2008
- Manuscript Accepted: 1 JUL 2008
- Manuscript Revised: 17 JUN 2008
- Manuscript Received: 28 APR 2008
- NIH Training. Grant Number: T32 NS07494-04
- fluorescent in situ hybridization
Glioblastomas exhibit a remarkable tendency toward morphologic diversity. Although rare, pseudoepithelial components (adenoid or epithelioid) or true epithelial differentiation may occur, posing a significant diagnostic challenge.
Hematoxylin and eosin–stained slides were reviewed, and immunohistochemistry and fluorescence in situ hybridization were performed.
The patients included 38 men and 20 women. The median age at diagnosis was 57 years (interquartile range [IQR], 50 years-67 years), and the median overall survival was 7 months (IQR, 4 months-11 months). “Adenoid” glioblastomas (A-GBM) predominated (48%). True epithelial glioblastomas (TE-GBM) were next most frequent based on morphology and immunohistochemistry (35%), followed by epithelioid glioblastomas (E-GBM) (17%). Overall, 25 (43%) tumors featured a sarcomatous component. Molecular cytogenetic abnormalities identified by fluorescent in situ hybridization in A-GBM, E-GBM, and TE-GBM, respectively, included p16 deletion/-9 (60%, 71%, 64%); chromosome 10 loss (40%, 63%, 57%), chromosome 7 gain without EGFR amplification (70%, 38%, 40%), EGFR amplification (10%, 50%, 27%), PTEN deletion (10%, 25%, 29%), PDGFRA amplification (10%, 25%, 0%), and RB1 deletion/−13q (50%, 0%, 14%). Abnormalities identified by immunohistochemistry included p21 immunonegativity (60%, 25%, 93%), which was most frequent in TE-GBM (P = .008), strong nuclear p53 staining (29%, 29%, 41%), strong membranous staining for epidermal growth factor receptor (EGFR) (21%, 63%, 19%), which was most frequent in E-GBM (P = .03), and an increased frequency of p27 immunonegativity in gliosarcomas (15% negative, 85% focal) compared with tumors without sarcoma (38% strongly positive) (P = .009).
Pseudoepithelial and true epithelial morphology are rare phenomena in GBM and may be associated with a similar poor prognosis. These tumors demonstrate proportions of molecular genetic abnormalities varying somewhat from conventional GBM. Cancer 2008. © 2008 American Cancer Society.