bromochloroacetic-acid and Glioblastoma

Before entering human clinical studies to evaluate their safety and effectiveness, new drugs and novel medical treatments are subject to extensive animal testing that are expensive and time-consuming. By contrast, advanced technologies enable the development of animal-free models that allow the efficacy of innovative therapies to be studied without sacrificing animals, while providing helpful information and details. We report on the powerful combination of 3D bioprinting (3DB) and photo-thermal therapy (PTT) applications. To this end, we realize a 3DB construct consisting of glioblastoma U87-MG cells in a 3D geometry, incorporating biomimetic keratin-coated gold nanoparticles (Ker-AuNPs) as a photo-thermal agent. The resulting plasmonic 3DB structures exhibit a homogeneous cell distribution throughout the entire volume while promoting the localization of Ker-AuNPs within the cells. A 3D immunofluorescence assay and transmission electron microscopy (TEM) confirm the uniform distribution of fluorescent-labeled Ker-AuNPs in the volume and their capability to enter the cells. Laser-assisted (λ = 532 nm) PTT experiments demonstrate the extraordinary ability of Ker-AuNPs to generate heating, producing the highest temperature rise of about 16 °C in less than 2 min.

Topics: Biomimetic Materials; Glioblastoma; Gold; Humans; Hyperthermia, Induced; Keratins; Metal Nanoparticles; Photothermal Therapy

Topics: Biomimetics; Glioblastoma; Gold; Humans; Keratins; Metal Nanoparticles; Photothermal Therapy

Gamma-glutamyltransferase (GGT) and keratins (KRT) are key factors in regulating tumor progression rely on emerging evidence. However, the prognostic values of GGT and KRT isoforms and their regulation patterns at transcriptional and post-transcriptional levels have been rarely studied. In this study, we aimed to identify cooperative prognostic biomarker signature conducted by GGT and KRT genes for overall survival prediction and discrimination in patients with low-grade glioma (LGG) and glioblastoma multiforme (GBM). To this end, we employed a differential expression network analysis on LGG-NORMAL, GBM-NORMAL, and LGG-GBM datasets. Then, all the differentially expressed genes related to a GO term "GGT activity" were excluded. After that, for obtained potential biomarkers genes, differentially expressed lncRNAs were used to detect cis-regulatory elements (CREs) and trans-regulatory elements (TREs). To scrutinize the regulation on the cytoplasm, potential interactions between these biomarker genes and DElncRNAs were predicted. Our analysis, for the first time, revealed that GGT6, KRT33B, and KRT75 in LGG, GGT2, and KRT75 in GBM and KRT75 for LGG to GBM transformation tumors can be novel cooperative prognostic biomarkers that may be applicable for early detection of LGG, GBM, and LGG to GBM transformation tumors. Consequently, KRT75 was the most important gene being regulated at both transcriptional and post-transcriptional levels significantly. Furthermore, CREs and their relative genes were coordinative up-regulated or down-regulated suggesting CREs as regulation points of these genes. In the end, up-regulation of most DElncRNAs that had physical interaction with target genes pints out that the transcripted genes may have obstacles for translation process.

Topics: Biomarkers, Tumor; Brain Neoplasms; gamma-Glutamyltransferase; Gene Expression Regulation, Neoplastic; Glioblastoma; Glioma; Humans; Keratins; Protein Isoforms

Currently used glioblastoma cultures have many disadvantages and are being replaced by short-term cultures. However, these may include normal brain cells.. A comparative model of normal and glioma cultures is lacking. A significant contributory factor is because cultures from adult human brain contain small amounts of cells with glial phenotypes. The predominant population of flat or spindle shaped cells does not express glial markers and are often termed as "glia-like".. Cryopreserved glioblastoma cultures from 28 bioptic samples were examined by immunofluorescence using antibodies to intermediate filaments (IF): glial fibrillary acidic protein (GFAP), cytokeratins (CK), nestin (Nes), vimentin (Vim) and neurofilaments (NF).. In short-term glioblastoma cultures GFAP-positive cells occured at higher percentages in 3/28 cultures and in lower percentages in further 5 cultures. Subpopulation of nestin positive cells were observed in all cultures and CK-positive cells were found in 25/28 cultures. All cells in all cultures were positively stained only for vimentin and negatively for NF. Cells grew slowly in 5 cultures which showed early proliferation arrest between passages 7 to 8. A further 23 cultures showed growth arrest by passages 10 to 15.. The presence of normal cells in short-term glioblastoma cultures may be caused by the infiltrative growth of these tumors. Our comparative analysis of morphological, growth and cytoskeletal properties revealed similarities between glioblastoma and normal brain cultures. In this study, the majority (28/30) of short-term glioblastoma showed limited life spans, similar to normal cells lacking spontaneous immortalization. The use of short-term glioblastoma cultures has two main problematic areas: cultures may contain a major subpopulation of normal "glia-like" cells; or they may contain the inital phases of spontaneously immortalized glioblastoma cells bearing properties of permanent cell lines (Tab. 1, Fig. 2, Ref. 19).

Topics: Brain Neoplasms; Glial Fibrillary Acidic Protein; Glioblastoma; Glioma; Humans; Intermediate Filaments; Keratins; Nestin; Neuroglia; Tumor Cells, Cultured; Vimentin

Glioblastoma multiforme (GBM), one of the most aggressive tumors in humans, is highly angiogenic. However, treatment with the angiogenesis inhibitor bevacizumab has not significantly prolonged overall patient survival times. GBM resistance to angiogenesis inhibitors is attributed to multiple interacting mechanisms. Although mesenchymal transition via glioma stem-like cells has attracted attention, it is considered a poor biomarker. There is no simple method for differentiating tumor-derived and reactive vascular cells from normal cells. The authors attempted to detect the mesenchymal transition of tumor cells by means of p53 and isocitrate dehydrogenase 1 (IDH1) immunohistochemistry.. Using antibody against p53 and IDH1 R132H, the authors immunohistochemically analyzed GBM tissue from patients who had undergone surgery at the University of Miyazaki Hospital during August 2005-December 2011. They focused on microvascular proliferation with a p53-positive ratio exceeding 50%. They compared TP53 mutations in original tumor tissues and in p53-positive and p53-negative microvascular proliferation cells collected by laser microdissection.. Among 61 enrolled GBM patients, the first screening step (immunostaining) identified 46 GBMs as p53 positive, 3 of which manifested areas of prominent p53-positive microvascular proliferation (>50%). Histologically, areas of p53-positive microvascular proliferation tended to be clustered, and they coexisted with areas of p53-negative microvascular proliferation. Both types of microvascular proliferation cells were clearly separated from original tumor cells by glial fibrillary acidic protein, epidermal growth factor receptor, and low-/high-molecular-weight cytokeratin. DNA sequencing analysis disclosed that p53-positive microvascular proliferation cells exhibited TP53 mutations identical to those observed in the original tumor; p53-negative microvascular proliferation cells contained a normal allele. Although immunostaining indicated that 3 (2 primary and 1 secondary) of the 61 GBMs were positive for IDH1, no tumors contained microvascular proliferation cells positive for IDH1 R132H.. Some microvascular proliferation clusters in GBM result from mesenchymal transition. The identification of useful markers might reveal this phenomenon as an infrequent event in GBMs.

Topics: Biomarkers, Tumor; Blood Vessels; Brain Neoplasms; Cell Proliferation; Epithelial-Mesenchymal Transition; ErbB Receptors; Female; Gene Expression Regulation, Neoplastic; Glial Fibrillary Acidic Protein; Glioblastoma; Humans; Isocitrate Dehydrogenase; Keratins; Male; Middle Aged; Mutation; Retrospective Studies; Tumor Suppressor Protein p53

Little is known about the cytokeratin (CK) expressions in glioblastoma multiforme (GBM). The aim is to explore the CK expression in GM using immunohistochemistry (IHC). IHC study in 30 cases (median = 68 years, SE = 12.6) of GBM in brain. CK expression using AE1/3 antidody was seen in 29/30 (97 %) cases. There were no expressions of CK34BE12, CK5, CK6, CK7, CK8, CK14, CK 18, CK19, and CK20. Expression of p53 and glial fibrillary acidic protein (GFAP) were recognized in all 30 cases (100 %). All cases showed Ki-67 antigen labeling, index of which ranged from 6 to 43 % (m ± SD = 24 + 16). The IHC using CKAE1/3 in GBM very frequently shows positive reaction. The expression may cause difficulty in pathologic diagnosis in GBM, particularly in discrimination between GBM and metastatic carcinoma. The CK positivity in GM may be due to CK molecules other than CK34BE12, CK5, CK6, CK7, CK8, CK14, CK18, CK19 and CK20. GBM frequently expression p53 and high Ki-67 labeling.

Topics: Aged; Biomarkers, Tumor; Brain Neoplasms; Female; Follow-Up Studies; Glioblastoma; Humans; Immunoenzyme Techniques; Keratins; Ki-67 Antigen; Male; Neoplasm Grading; Prognosis

Cerebrospinal fluid (CSF) cytology provides valuable diagnostic and prognostic information for diseases of the central nervous system (CNS) and remains the gold standard for the detection of neoplastic meningitis. Metastatic involvement of the CSF by non-CNS neoplasms far surpasses that of primary brain tumors, although conventional glioblastoma multiforme (GBM) can occasionally be identified in the CSF. GBM with epithelial differentiation is an uncommon variant that may contain features such as adenoid structures, signet ring cells, or squamous metaplasia. Herein, we present a case of GBM with epithelial differentiation to highlight a potential diagnostic pitfall in CSF cytology. A 55-year-old man presented with neurological symptoms and a 6.4 cm left temporal lobe cystic mass. Primary resection revealed GBM with focal epithelial differentiation confirmed by cytokeratin, epithelial membrane antigen, and glial fibrillary acidic protein immunohistochemical studies. Four months following primary resection, the patient developed severe headache for which a lumbar puncture with CSF cytologic evaluation was performed. The cytospin preparation showed numerous malignant epithelioid cells with high nuclear-cytoplasmic ratio and prominent cytoplasmic vacuoles resembling metastatic carcinoma. However, the lesional cells were cytomorphologically identical to the epithelial component present in the patient's recently diagnosed GBM. This case illustrates the potential for GBM with epithelial differentiation to closely mimic metastatic carcinoma from a non-CNS site in CSF cytology, which expands the differential diagnosis and emphasizes the necessity of clinical correlation.

Topics: Biomarkers, Tumor; Brain Neoplasms; Carcinoma in Situ; Cell Differentiation; Diagnosis, Differential; Epithelial Cells; Glial Fibrillary Acidic Protein; Glioblastoma; Humans; Keratins; Male; Middle Aged; Mucin-1; Neuroglia; Radiography; Temporal Lobe

Metastatic carcinoma, which is a common malignant tumor seen in the central nervous system is often difficult to distinguish from glioblastoma multiforme. In general, neoplastic cells maintain fidelity in the expression of parent cell intermediate filament and immunohistochemistry remains the mainstay in diagnosis. A panel consisting of GFAP (usually positive for astrocytic tumors) and cytokeratin (usually positive for metastatic carcinomas) is most commonly used for this purpose. However, co-expression of two or more classes of intermediate filament proteins by neoplasms is a widespread phenomenon and there are reports of glial neoplasms expressing keratin markers. Our aims and objectives were to analyse the expression of both cytokeratin and GFAP in different glial tumors and metastatic carcinomas. Cases were collected for a period of two years. All the cases were diagnosed as primary or metastatic intracranial tumors. Formalin-fixed paraffin-embedded thin sections were taken on egg-albumin coated slides and immunostaining with GFAP and polyclonal cytokeratin was done. Forty-five tumors were analysed, including 35 glial neoplasms and 10 metastatic carcinomas of which 7 of the 32 astrocytic neoplasms (22%) showed focal immunoreactivity with pancytokeratin. All of the glial tumors but none of the metastatic carcinomas were positive with GFAP. So our conclusion was that co-expression of GFAP and CK is a fairly common phenomenon, especially in case of undifferentiated and high grade gliomas and this must be kept in mind while differentiating these cases from metastatic carcinoma, as CK positivity does not rule out the diagnosis of a glial neoplasm. Further studies with an expanded panel of CK is most useful for this.

Topics: Astrocytoma; Biomarkers, Tumor; Brain Neoplasms; Carcinoma; Diagnosis, Differential; Glial Fibrillary Acidic Protein; Glioblastoma; Glioma; Humans; Immunohistochemistry; Keratins; Oligodendroglioma

Two metachronous glioblastomas with different cerebral locations in a 53-year-old long-term survival patient were analyzed by multiple genetic approaches. Using comparative genomic hybridization a different pattern of chromosomal aberrations was observed, with 19 imbalances in the first tumor and only 2 imbalances in the second. Sequence analysis revealed a distinct mutation profile in each tumor, with amino acid substitutions in the p53 and PTEN genes only in the first tumor, ie, p53 in codon 273 (CGT-->TGT, Arg-->Cys) and PTEN in codon 336 (TAC-->TTC, Tyr-->Phe). A splicing acceptor site PTEN mutation (IVS8-2A>G) was observed only in the second GBM. EGFR amplification, mutations of p16INK4a/CDKN2A or p14ARF were not observed. According to the results of p53 mutational analysis and EGFR amplification studies, the first tumor is classified as a type 1 GBM, whereas the alterations in the second one are different from those typically encountered in type 1 or type 2 tumors. In conclusion, our data strongly suggest that the metachronous tumors in this patient are exceptional in that they developed independently from each other. Whether the molecular features of the first glioblastoma are associated with the notably extended recurrence-free period of 5 years remains to be elucidated.

Topics: Brain Neoplasms; Chromosome Mapping; Chromosomes, Human, Pair 10; Cyclin-Dependent Kinase Inhibitor p16; DNA Mutational Analysis; DNA-Binding Proteins; Genes, erbB-1; Glial Fibrillary Acidic Protein; Glioblastoma; Humans; Immunohistochemistry; Keratins; Ki-67 Antigen; Loss of Heterozygosity; Magnetic Resonance Imaging; Male; Middle Aged; MutS Homolog 2 Protein; Neoplasms, Second Primary; Nerve Tissue Proteins; Phosphoric Monoester Hydrolases; Polymerase Chain Reaction; Proto-Oncogene Proteins; PTEN Phosphohydrolase; S100 Proteins; Sequence Analysis, DNA; Staining and Labeling; Tumor Suppressor Protein p53; Tumor Suppressor Proteins; Vimentin

Glial fibrillary acidic protein (GFAP), vimentin (Vi) and cytokeratin (CK) intermediate filament (IF) proteins were studied in glioblastoma cell line GL-15. The immunofluorescence staining revealed strong positive staining for vimentin in all cultured cells. Approximately 20% of analyzed cells showed strong and 50% moderate intensity of staining for GFAP. About 3% of all cells were positively stained with a mixture of anti-CK monoclonal antibodies. The expression of all IF was not in relation to the cell density or days in vitro after passage. The double immunofluoresce revealed that all CK-positive cells express GFAP and vimentin. This study demonstrates the heterogeneity of the clonal GL-15 glioma cell line which consists in three immunocytochemically distinct cell types: Vi+/GFAP-/CK-, Vi+/GFAP+/CK-, and Vi+/GFAP+/CK+. These findings give further evidence about the expression of non-glial IF in cultured glioma cells.

Topics: Brain Neoplasms; Glial Fibrillary Acidic Protein; Glioblastoma; Humans; Keratins; Microscopy, Fluorescence; Tumor Cells, Cultured; Vimentin

Poorly differentiated metastatic carcinoma may be difficult to distinguish histologically from high-grade astrocytic malignant neoplasms, particularly on small open or stereotactic biopsy specimens. Previous authors have reported that a subset of glioblastoma multiforme (GBM) variably stains with cytokeratin immunomarkers. The authors examined a panel of epithelial and keratin antibodies by paraffin immunohistochemistry to evaluate the immunophenotype of GBM for these markers and to determine what combination of immunostains would be optimal in distinguishing GBM from metastatic carcinoma.. Twenty-three patients with GBM (age range, 19-86 years; mean, 63.4 years; 14 men and 9 women) and 22 patients with metastatic carcinoma (age range, 26-77 years; mean, 58.1 years; 7 men and 15 women) to the brain were studied with a panel of immunostains, including glial fibrillary acid protein (GFAP), Ber-EP4, antikeratin monoclonal antibodies AE1/3, and antibodies to CAM 5.2 and cytokeratins 7 (CK7) and 20 (CK20). Sites of origin for the metastatic tumors included lung (n = 11), breast (n = 5), endometrium (n = 1), prostate (n = 1), colon (n = 1), presumed kidney (n = 1), and unknown (n = 2).. All GBMs stained positive for GFAP (100%), and all but 1 (95.7%) stained positive for cytokeratins AE1/3. Only rare focal immunoreactivity was observed in a single case of GBM with CAM 5.2 (4.3%), CK7 (4.3%), and CK20 (4.3%). Immunoreactivity with Ber-EP4 was not observed in any of the GBMs (0.0%). All cases of metastatic carcinoma stained positive with cytokeratins AE1/3 (100%) and CAM 5.2 (100%). Variable staining was observed in carcinomas with CK7 (17 of 22, 77.3%), Ber-EP4 (11 of 22, 50.0%), and CK20 (9 of 22, 40.9%). Three metastatic carcinomas showed rare GFAP-positive staining cells (13.6%).. Based on the aforementioned results, a combination of immunostains, including GFAP and cytokeratin CAM5.2, may be the most useful in differentiating poorly differentiated metastatic carcinoma from GBM. A significant number of GBMs stain with some cytokeratin markers, in particular cytokeratins AE1/3. Because of the poor specificity of cytokeratins AE1/3 in distinguishing metastatic carcinoma from GBM, it should not be used to differentiate the 2 entities.

Topics: Adult; Aged; Aged, 80 and over; Antigens, Neoplasm; Biomarkers, Tumor; Brain Neoplasms; Cell Adhesion Molecules; Female; Glial Fibrillary Acidic Protein; Glioblastoma; Humans; Immunoenzyme Techniques; Keratins; Male; Middle Aged

Intracranial nervous-system tumours were diagnosed in three of 1092 bovine necropsy specimens submitted to the Department of Veterinary Pathology, Obihiro University between April 1983 and March 1996. A fourth case was a referral from the Department of Veterinary Pathology, Rakuno Gakuen University. Histopathological examination revealed four types of tumour: intracranial malignant peripheral nerve sheath tumour (MPNST), choroid plexus papilloma, differentiated fibrillary astrocytoma and anaplastic (malignant) astrocytoma. Immunohistochemically, the intracranial MPNST was strongly positive for S-100 protein and vimentin, and in places weakly positive for glial fibrillary acid protein (GFAP). The choroid plexus papilloma was strongly positive for epithelial membrane antigen (EMA), keratin, S-100 protein and vimentin, and positive for GFAP in places. The cytoplasm and fibrous component in the differentiated fibrillary astrocytoma were strongly positive for S-100 protein and GFAP. The anaplastic (malignant) astrocytoma was strongly positive for vimentin, S-100 protein and keratin in the cytoplasm and fibrous processes, and weakly positive for GFAP and EMA in places. Myelin basic protein (MBP) and synaptophysin showed a weak positive reaction in the marginal areas of the tumour.

Topics: Animals; Astrocytoma; Brain Neoplasms; Cattle; Cattle Diseases; Glial Fibrillary Acidic Protein; Glioblastoma; Glioma; Immunohistochemistry; Keratins; Mucin-1; Myelin Basic Protein; Nerve Sheath Neoplasms; S100 Proteins; Vimentin

In this study, 29 formalin-fixed, paraffin-embedded astrocytic tumors were analyzed immunocytochemically with the antikeratin monoclonal antibodies Mak-6 and Cam 5.2 and a polyclonal antibody against glial fibrillary acidic protein (GFAP). Immunoreactivity for Mak-6 was present in 29 cases (100%) including six well-differentiated astrocytomas, nine anaplastic astrocytomas, and 14 glioblastomas multiforme. Cam 5.2 immunoreactivity was focally present in one case of GBM (4%) but was absent in the remaining 28 cases. All cases were immunoreactive with an antibody against GFAP. Cytokeratin (CK) expression was examined in extracts of four separate well-characterized astrocytoma cell lines by Western blotting with the monoclonal antibodies Mak-6, Cam 5.2, and anti-CK 18 and by Northern analysis using a cDNA probe for the human CK 18 gene. The Western blots revealed the presence of immunoreactive bands corresponding to CK numbers 14/15, 16, and 18 in extracts from all four cell lines and additional bands corresponding to CK 8 in 3/4 lines and CK 19 in 1/4 lines. Northern analysis detected CK 18 mRNA in extracts from 2/4 astrocytic cell lines. These findings demonstrate that CK immunoreactivity is frequent in astrocytic tumors and confirm through the molecular and biochemical analysis of CK 18 gene expression and of keratin intermediate filament proteins that the basis for CK immunoreactivity in astrocytic tumors is bona fide CK expression, not cross-reactivity with other antigens or artifact. The demonstration of CK expression by astrocytic neoplasms has important implications for pathologists involved in the diagnosis of poorly differentiated tumors.

Topics: Antibodies, Monoclonal; Astrocytoma; Blotting, Northern; Blotting, Western; Glial Fibrillary Acidic Protein; Glioblastoma; Humans; Immunohistochemistry; Keratins; Paraffin Embedding; Tumor Cells, Cultured

The Cavitron ultrasonic surgical aspirator (CUSA) is a dissecting system that allows quick and effective removal of CNS tumors without traction or excessive manipulation of normal tissue. In this article, the immunoperoxidase staining patterns of cytology specimens obtained with the CUSA are compared with those from their corresponding resected surgical specimens employing a battery of monoclonal and polyclonal antibodies. Eleven cases of meningioma, three cases of glioblastoma multiforme, one astrocytoma, and two schwannomas were evaluated. In both CUSA cytologic biopsies and surgical biopsies, all the meningiomas showed strong staining for vimentin and epithelial membrane antigen, while two showed focal staining for cytokeratins. The glioblastoma multiforme and astrocytoma cases showed positivity for vimentin, S-100 protein, and glial fibrillary acidic protein, while the schwannomas stained positively for vimentin and S-100 protein. With only rare exceptions, the immunocytochemistry of the CUSA and surgical specimens correlated well in all of these cases in terms of strength of reaction and localization. There were no false-positive staining reactions in the CUSA material. This study suggests that reliable morphologic and immunoperoxidase studies can be performed on cytologic material obtained by the CUSA, which could aid in making an accurate and specific diagnosis of a variety of CNS tumors.

Topics: Astrocytoma; Biopsy; Cytodiagnosis; Glial Fibrillary Acidic Protein; Glioblastoma; Humans; Immunoenzyme Techniques; Keratins; Meningioma; Neoplasms, Nerve Tissue; Neurilemmoma; Neurosurgery; S100 Proteins; Suction; Ultrasonic Therapy; Vimentin

Immunohistochemical analysis of 30 paraffin-embedded astrocytic neoplasms was performed to correlate the expression of intermediate filament proteins with histologic subtype. Each tumor was studied with monoclonal antibodies to keratin, vimentin, desmin, 200-kd neurofilament protein, and glial fibrillary acidic protein (GFAP). Immunoreactivity with the anti-keratin monoclonal antibodies AE1 and AE3 was demonstrated in 24 cases (80%) including 4 of 6 (66%) well-differentiated astrocytomas (WDAs), 10 of 12 (83%) anaplastic astrocytomas (ANAs), and 10 of 12 (83%) glioblastomas multiforme (GBMs). These cases were further studied with the monoclonal antikeratin antibodies 34 beta E12 and 34 beta H11. Of the 24 AE1/AE3-positive cases, 14 (58%) reacted with 34 beta E12. None of the cases was reactive with 34 beta H11. Vimentin expression was demonstrated in 24 cases (80%), including 2 of 6 (33%) WDAs, 11 of 12 (92%) ANAs, and 11 of 12 (92%) GBMs. Coexpression of keratin and vimentin was observed in 20 cases (67%), including 2 of 6 WDAs, 9 of 12 (75%) ANAs, and 9 of 12 (75%) GBMs. Immunoreactivity with GFAP antibody was present in all 30 (100%) cases, but none of the tumors was reactive with antibodies to desmin or 200-kd neurofilament protein. These findings demonstrate that expression of both keratin and vimentin intermediate filaments is common in astrocytic neoplasms regardless of histologic grade.

Topics: Astrocytoma; Biomarkers, Tumor; Glial Fibrillary Acidic Protein; Glioblastoma; Humans; Immunoenzyme Techniques; Intermediate Filament Proteins; Keratins; Staining and Labeling; Vimentin

Monoclonal antibodies (AE1/3, CAM 5.2 and PKK-1) and polyclonal antisera against the cytokeratin proteins were reacted with a range of astrocytic tumours, oligodendrogliomas and ependymomas. Seven of 12 cases (58%) of glioblastoma multiforme, five of eight (63%) anaplastic astrocytomas and two of five (40%) well-differentiated astrocytomas were immunoreactive with AE1/3 but not with the other anti-cytokeratin antibodies. In oligodendrogliomas, AE1/3 stained isolated astrocyte-like cells as well as scattered neoplastic oligodendrocytes in four of eight cases (50%) cases. Four ependymomas were negative for all cytokeratin markers examined. The immunostaining of astrocytomas and oligodendrogliomas with AE1/3 might represent co-expression of cytokeratin with glial fibrillary acidic protein by gliomas and calls for caution in the use of these antibodies in the differential diagnosis between gliomas and carcinomas.

Topics: Adult; Antibodies, Monoclonal; Astrocytoma; Child; Glioblastoma; Humans; Immunohistochemistry; Keratins; Oligodendroglioma