scholarly journals Immunohistochemical expression of glial fibrillary acidic protein and CAM5.2 in glial tumors and their role in differentiating glial tumors from metastatic tumors of central nervous system

2015 ◽  
Vol 06 (04) ◽  
pp. 499-503 ◽  
Author(s):  
Rama Goyal ◽  
Satyavir Kumar Mathur ◽  
Sumiti Gupta ◽  
Rahul Goyal ◽  
Sanjay Kumar ◽  
...  

ABSTRACT Background and Objectives: Immunohistochemistry (IHC) has become an important tool in the diagnosis of metastatic brain tumors. The judicious use of a panel of selected immunostains is unquestionably helpful in diagnostically challenging cases. In our study, the best combination of immune markers useful in differentiating metastatic carcinoma from high-grade gliomas in central nervous system (CNS) are glial fibrillary acidic protein (GFAP) and cytokeratin (CK) (CAM5.2). Materials and Methods: The study was conducted on 80 cases of glial tumors including metastatic tumors to the CNS. Histopathological diagnosis was established on routine hematoxylin and eosin staining of the sections. Special IHC markers, GFAP, and CAM5.2 were used to differentiate glial from metastatic tumors. Result: Of total 80 cases, 40 cases of astrocytic tumors, 2 cases of ependymoma, 2 cases of mixed glial tumors, and 16 cases of glioblastoma multiforme were positive for GFAP. Twelve cases of oligodendroglioma were negative for GFAP. The sensitivity of GFAP in glial tumors was statistically significant as 81.1% and specificity 100%, whereas sensitivity and specificity of CAM5.2 in metastatic tumors were 100%. Conclusion: IHC plays an important role in diagnosing tumors of CNS and markers such as GFAP and CK (CAM5.2) are quite effective in differentiating glial tumors from metastatic tumors of CNS.

Neurosurgery ◽  
2003 ◽  
Vol 53 (3) ◽  
pp. 743-748 ◽  
Author(s):  
George M. Kleinman ◽  
David Zagzag ◽  
Douglas C. Miller

Abstract OBJECTIVE To describe the pathological features of three very similar and unusual primary central nervous system tumors that are not readily recognized as conventional ependymomas but which, by ultrastructural examination, have an ependymomatous character. METHODS Three distinctive tumors were found in a review of our files for cases of ependymoma. In each case, hematoxylin and eosin-stained sections were reviewed, and immunostains for epithelial membrane antigen, cytokeratin, vimentin, and glial fibrillary acidic protein were performed on formalin-fixed, paraffin-embedded sections. Electron microscopy was performed in each case. RESULTS The tumors had a diffuse myxoid background, often containing tightly clustered cells that mimicked multinucleated giant cells, but lacking perivascular pseudorosettes or central lumen rosettes. Glial fibrillary acidic protein and vimentin immunostains did not reveal perivascular processes. Epithelial membrane antigen immunostains showed a dot-like cytoplasmic immunoreactivity in some cell clusters in two of the three cases. Cytokeratin was negative in all three cases. However, ultrastructurally, the cells of each tumor had extensive surface microvilli; the giant cell-like clusters had cells with extensive close appositions, some junctions, and, in two cases, lumina with microvilli. Two of the patients were adults (both with temporal lobe tumors), and one patient was 13 years old and had a cervical spinal cord intramedullary tumor. Each tumor was sharply circumscribed from adjacent central nervous system tissue but was not encapsulated. One of the cases in an adult was mitotically highly active; this tumor recurred locally 4 years after initial gross total excision. CONCLUSION These tumors are unusual variants of ependymoma. This pattern of ependymoma is sufficiently distinctive to be recognized in hematoxylin and eosin stains once the architecture of the epithelioid clusters is appreciated.


Author(s):  
Albee Messing

Abstract Background Alexander disease is caused by dominantly acting mutations in glial fibrillary acidic protein (GFAP), the major intermediate filament of astrocytes in the central nervous system. Main body In addition to the sequence variants that represent the origin of disease, GFAP accumulation also takes place, together leading to a gain-of-function that has sometimes been referred to as “GFAP toxicity.” Whether the nature of GFAP toxicity in patients, who have mixtures of both mutant and normal protein, is the same as that produced by simple GFAP excess, is not yet clear. Conclusion The implications of these questions for the design of effective treatments are discussed.


1999 ◽  
Vol 145 (3) ◽  
pp. 503-514 ◽  
Author(s):  
Milos Pekny ◽  
Clas B. Johansson ◽  
Camilla Eliasson ◽  
Josefina Stakeberg ◽  
Åsa Wallén ◽  
...  

In response to injury of the central nervous system, astrocytes become reactive and express high levels of the intermediate filament (IF) proteins glial fibrillary acidic protein (GFAP), vimentin, and nestin. We have shown that astrocytes in mice deficient for both GFAP and vimentin (GFAP−/−vim−/−) cannot form IFs even when nestin is expressed and are thus devoid of IFs in their reactive state. Here, we have studied the reaction to injury in the central nervous system in GFAP−/−, vimentin−/−, or GFAP−/−vim−/− mice. Glial scar formation appeared normal after spinal cord or brain lesions in GFAP−/− or vimentin−/− mice, but was impaired in GFAP−/−vim−/− mice that developed less dense scars frequently accompanied by bleeding. These results show that GFAP and vimentin are required for proper glial scar formation in the injured central nervous system and that some degree of functional overlap exists between these IF proteins.


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