Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antigen expression in a human glioblastoma was investigated by immunochemical methods in the primary tumor, the first and second recurrence, a permanent cell line derived from the first recurrence and in its xenotransplantation tumors. In the primary tumor, GFAP, vimentin, S100, Leu-7 and glioma-associated antigens (GAA) as defined by the monoclonal antibodies (mAbs) MUC 2-39, MUC 8-22 and MUC 2-63 were markedly expressed. In the recurrences, gradual loss of GFAP and Leu-7 could be observed, whereas S100, vimentin and GAA gave similar results to those in the primary tumor. In contrast, fibronectin and collagen IV, which were restricted to the vessel walls in the primary tumor, were represented in sarcomatous areas of the recurrences. In some of these areas, co-expression of glial cell markers was observed. In short-term cell cultures, expression of glia- and glioma-associated antigens as well as fibronectin and collagen IV was comparable to that of the recurrent tumor tissue. In long-term passages, immunoreactivity of GFAP, Leu-7 and S100 decreased, whereas GAA, vimentin and fibronectin increased. Collagen IV positive cells were not visible beyond passage 15. Transplantation tumors were only partly positive for glial cell markers, but revealed strong immunoreactivity for GAA, fibronectin and collagen IV. With these observations we confirm that the phenotypic variability of glioma cells makes it difficult to identify the origin of cells in human glioblastomas from their antigenicity.
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PMID:Antigen variation in a human glioblastoma: from the primary tumor to the second recurrence, permanent cell line and xenotransplantation tumors. 206 11

The authors describe an autopsy case of glioblastoma occurred after 38 years received lobotomy. The patient was a 72 year-old male, who received lobotomy at 34 year old against schizophrenia. CT scan taken at 72 year old showed irregular low density areas without mass effect in the bilateral frontal white matter adjacent to the anterior horn. After 4 months, the signs of intracranial hypertension were observed and his consciousness was disturbed abruptly. CT scan revealed ring enhancement with marked mass effect in the left frontal lobe. A biopsy specimen from the tumor showed a picture of anaplastic astrocytoma. Family rejected the remission maintenance treatment. The patient died 3 months later the onset. At autopsy, a large tumor occupied in the left frontal lobe was recognized. The tumor demarcated poorly from the cerebral tissue and invaded into the left anterior cingulate gyrus and the corpus callosum. Histologically, tumor cells composed of fibrillary, gemistocytic and multinucleated astrocytes. GFAP, NSE and vimentin were found in large cells. Histological diagnosis was glioblastoma. It was suggested that the tumor occurred from the region around a cyst of prefrontal lobotomy in the left frontal lobe. In the right frontal lobe, a large cyst in size of 30-18 mm was present in the centrum semiovale. The wall of cyst was composed of layer of glial scar tissue. The origin of the cyst was discussed.
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PMID:[An autopsy case of glioblastoma occurred in the region after lobotomy]. 207 52

Glioblastomas are generally thought to be more common in men than in women. In order to investigate the hormone-dependence of these tumours, we established a human glioblastoma line in athymic mice. The tumour cell type was characterized using immunocytochemical methods. The influence of host sex on growth was evaluated, and hormone receptors were characterized biochemically. The histological features of the initial tumour were conserved in the hetero-transplanted tumours, which consisted of vimentin and GFAP immunoreactive astrocytes. There was a highly significant difference in tumour growth between the two sexes (P less than 0.01). In the male mice, tumours were from 2.5 to 10 times larger than in the females, the latency periods were 30% shorter, and the growth phases were characterized by periods of slow or zero growth. In addition, androgen and oestrogen receptors were detected at low levels (80-270 fmol/g tumour) in the heterotransplanted tumours especially in the males. The fact that the male tumour growth profiles resembled those of some hormone-dependent lines, and that androgen receptors were found preferentially in the male rather than in female tumours would tend to indicate that there is a hormonal influence on the growth of the heterotransplanted tumours. These results provide further evidence for an influence of sex-steroid hormones on the growth of glioblastomas.
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PMID:Influence of host sex on the growth of a human glioblastoma line in athymic mice. 216 Oct 85

The immunocytochemical staining patterns of cultured glioma cells were investigated. Fifty nine individual cases were stained at different in vitro ages for glial fibrillary acidic protein, fibronectin, galactocerebroside, HNK-1/Leu 7, A2B5, vimentin, factor VIII and A4. Histologically, the cases were composed of eight low-grade astrocytomas, 11 high-grade astrocytomas, four low-grade oligodendrogliomas, seven high-grade oligodendrogliomas and 29 glioblastomas. The 45 cases were analysed within the first 3 weeks of culture, many of them as primary cultures. In 11 cases stainings were performed repeatedly at intervals of up to 6 months. Glial fibrillary acidic protein staining was positive in most of the early cultures of astrocytomas (low and high grade) and glioblastomas; expression in more than 50% of the cells was found in 1 of 5 low-grade astrocytomas, 5 of 11 high-grade astrocytomas and 14 of 29 glioblastomas. Two of the high-grade astrocytomas were stained once more after 6 weeks in culture and were found to be only 1% positive for glial fibrillary acidic protein but strongly positive for fibronectin. The same was true for five of the glioblastoma cases. Two of these cases remained glial fibrillary acid protein positive and developed into stable permanent cell lines. Only one case started with 1% of glial fibrillary acidic protein positive cells and later developed into a 99% glial fibrillary acidic protein positive cell line. Neither HNK-1/Leu 7 expression nor A2B5 staining appeared to have a relationship to the glial fibrillary acidic protein staining. It was observed that glial fibrillary acidic protein and HNK-1/Leu 7 were both 100% in some cases but that later one of the two antigens disappeared but not the other. The amount of glial fibrillary acidic protein staining does not allow the prediction of A2B5 staining. The study shows that initiation of primary cultures on an extracellular matrix yields more glial fibrillary acidic protein positive cells in primary cultures than have been found in other studies. It is concluded that only a rigid standardization of culture conditions will ensure the validity of comparisons of in vitro data obtained in primary cultures.
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PMID:Antigenic staining patterns of human glioma cultures: primary cultures, long-term cultures and cell lines. 224 42

Seven human glioblastoma cell lines established in vitro from primary tumor explants were studied. A marked heterogeneity of glial fibrillary acidic protein was observed whereas vimentin was uniformly expressed by all cell lines. Indirect immunofluorescence and flow cytofluorometry revealed a heterogeneous distribution of surface GE 2 and CG 12 tumor-associated antigens (TAA's): three cell lines were positive (greater than 69% TAA-positive cells) and three cell lines were negative (less than 9% TAA-positive cells). One cell line (Hu 228) was moderately positive at early culture passages and subsequently acquired a TAA-negative phenotype. The difference in the relative amounts of surface TAA's of the three positive cell lines was less than twofold. In spite of the heterogeneous distribution of surface TAA's, all cell lines exhibited considerable amounts of intracellular TAA. Treatment with phorbol esters and density-dependent growth arrest decreased the percentage of the TAA-positive cells and the amount of cell-surface TAA's in one cell line (Hu 195). Interferon-gamma treatment in vitro increased the percentage of CG 12-positive cells by 12% and the amount of cell-surface CG 12 antigens by 38% as compared to untreated cells. The percentage of TAA-positive cells among phorbol ester-treated cells of the Hu 195 cell line was lowest 48 hours after treatment, but returned to normal values within the next 48 hours. Reduction of 3H-thymidine incorporation preceded the decrease in number of TAA-positive cells by about 18 hours. Two-color fluorescence analysis performed in positive cell lines for simultaneous determination of surface TAA's and deoxyribonucleic acid content or reactivity with the proliferation-associated Ki67 intracellular marker indicated that GE 2 and CG 12 antigens are expressed preferentially by actively proliferating glioma cells. The results of this study indicate the existence of two different phenotypes in cultured human glioblastoma cells: surface TAA-positive/cytosol TAA-positive and surface TAA-negative/cytosol TAA-positive cell populations. In addition, modulation of TAA expression was dependent on the cell-cycle differentiation stage, culture conditions, and proliferative state of the cells.
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PMID:Heterogeneity and modulation of tumor-associated antigens in human glioblastoma cell lines. 276 91

The occurrence of a glioblastoma with sarcoma, a gliosarcoma, in the left frontal-temporal area of a 49-year-old woman with a history of Thorotrast exposure, is described. Thorotrast-laden histiocytes and free Thorotrast material were found in both components of the tumor. An overlying, adherent dural cranial lesion was found to contain massive deposits of Thorotrast embedded in a dense fibrotic and sclerotic stroma with focal calcification. These features are typical of "Thorotrastoma." Thorotrast stains greenish-brown with hematoxylin and eosin and appears as refractile granular particles of relatively uniform size either within histiocytes or as free material. The radioactivity of the deposits was confirmed through the use of a scintillation counter, and 232 thorium was definitively identified though the use of scanning electron microscopy with energy-dispersive X-ray analysis. Immunohistochemical studies of the tumor demonstrated glial fibrillary acid protein (GFAP) immunoreactivity in areas of glioma and focal vimentin and actin immunoreactivity in areas of sarcoma. Thorotrast-associated lesions of the central nervous system (CNS) are infrequently reported, and a Thorotrast-associated gliosarcoma has not yet been reported. The use of Thorotrast, its radiobiology, and sequelae are reviewed with particular emphasis on lesions occurring in the CNS.
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PMID:Thorotrast-associated gliosarcoma. Including comments on thorotrast use and review of sequelae with particular reference to lesions of the central nervous system. 328 27

During studies to investigate the localization of Ia antigens in normal mouse kidney, a monoclonal antibody (Mab) specific for I-Ab by microcytotoxicity criteria was found to crossreact with a tissue antigen present in the glomeruli and vasculature of murine tissues, irrespective of their Ia haplotype, as well as in human kidneys. Immunofluorescence and immunoperoxidase studies of frozen tissue sections revealed that the antigen responsible for the crossreaction was present in the cytoplasm of glomerular epithelial cells and of smooth muscle of blood vessels. The immunofluorescence pattern of primary cultures of human glomerular epithelial cells and of a glioblastoma cell line indicated that the crossreactive antigen forms part of the cytoskeleton, and resembled the pattern observed with a monoclonal against vimentin, one of the intermediate filaments. Thus this Mab, which is directed against mouse alloantigen Ia.20 in microcytotoxicity was found to crossreact with a cytoskeletal component present in the mouse, as well as in human glomerular epithelial and smooth muscle cells.
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PMID:Crossreactions between an I-A allospecificity and the cytoskeleton of glomerular epithelium and of vascular smooth muscle. 329 57

The plexiform lesion in primary pulmonary hypertension is a glomeruloid structure forming channels in branches of the pulmonary artery. These lesions have been considered an abnormal growth of modified smooth muscle cells. We present immunohistochemical evidence in 10 cases of plexogenic pulmonary hypertension that the plexiform channels and the concentric obliterative arteriopathy associated with these channels represent abnormal growth of factor VIII-related antigen-positive endothelial cells. In addition, these cells strongly expressed vimentin, a growth- and differentiation-related intermediate filament. Morphologically and immunohistochemically, the lesions resembled the neovascularization associated with the brain tumor glioblastoma multiform. Furthermore, we noted an exclusively perivascular inflammatory cell infiltrate (but no vasculitis) in seven of the 10 cases with plexogenic arteriopathy composed of T cells, B cells, and macrophages. Our findings indicate that the plexiform lesion may result from a deregulated growth of endothelial cells. The presence of perivascular inflammatory cells suggested that cytokines and growth factors may further influence the development of the plexiform lesion.
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PMID:Exuberant endothelial cell growth and elements of inflammation are present in plexiform lesions of pulmonary hypertension. 1143 86

Non-glial intermediate filament (IMF) proteins, as well as glial fibrillary acidic protein (GFAP) and vimentin, were studied by immunohistochemistry in 24 gliomas including low grade astrocytoma, pleomorphic xanthoastrocytoma, anaplastic astrocytoma, glioblastoma, oligodendroglioma, ependymoma and ependymoblastoma, which were fixed in ethanol and embedded in paraffin. Cytoskeletal elements isolated from two glioblastomas were examined with immunoblot analysis. All tumors had GFAP-positive neoplastic cells and vimentin was also found in all the tumors except one oligodendroglioma. Twenty-three gliomas were immunostained with anti-desmin polyclonal antibody (DM-P), but anti-desmin monoclonal antibody reacted to only one glioblastoma. DM-P might crossreact with GFAP and vimentin. Cytokeratin expression was investigated with six antibodies. Twenty gliomas (83%) were positive for the antibody against epidermal keratin (CK-SE), however positive immunoreactivity varied from 58 to 8% with other cytokeratin antibodies. With the Western blot method, CK-SE had protein bands at 53 and 60-66 kDa. Neurofilament was expressed in one pleomorphic xanthoastrocytoma, one anaplastic astrocytoma, one glioblastoma and one ependymoblastoma. Expression of nonglial IMF proteins were observed in 21 tumors (88%), and coexpression of 4 or 5 classes of IMF proteins in 3 tumors (13%). We conclude that, in addition to GFAP and vimentin, gliomas express several types of non-glial IMF proteins.
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PMID:Expression of non-glial intermediate filament proteins in gliomas. 751 71

Possible differentiation mechanisms were investigated in a glioblastoma multiform cell line (GL15) presenting an undifferentiated phenotype with weak glial fibrillary acidic protein (GFAP) and strong vimentin (VIM) expression. Serum-free conditions induced time-dependent increases of GFAP-mRNA and GFAP protein levels, associated with a process-bearing astrocytic morphology. Activation of protein kinase C (PKC) by tumor promoter phorbol 12-myrystate 13-acetate (PMA) induced a rapid morphological differentiation and a decrease in GFAP mRNA, whereas the GFAP level remained unchanged. Such parameters were shown to characterize a physiological differentiation stage in astroglial cultures. Treatment of process-bearing GL15 cells with dibutyryl cyclic AMP (dbcAMP), a protein kinase A (PKA) activator, induced a time-dependent decrease in the GFAP mRNA and GFAP protein levels and reverted morphological changes induced by serum-free conditions. Neither PMA nor dbcAMP influenced the VIM mRNA expression. In GL15 cells, PKC and PKA activation have opposite effects. Understanding the role of these kinases in malignant transformation and in the in vitro differentiation process is of both basic and clinical interest.
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PMID:PKA and PKC activation induces opposite glial fibrillary acidic protein (GFAP) expression and morphology changes in a glioblastoma multiform cell line of clonal origin. 754 74


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