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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenal chromaffin cells from early postnatal rats maintained in culture have previously been shown to grow neuritic processes and survive better in the presence of nerve growth factor (NGF). In the present study we have quantitated the effects on chromaffin cell (postnatal day (D) 8) survival and neurite outgrowth of: NGF, ciliary neuronotrophic factor (CNTF), activities contained in various types of conditioned media (CM), and various substrata (laminin, fibronectin and polyornithine-binding neurite-promoting factor from RN 22 Schwannoma cells - PNPF). At saturating concentrations CNTF (50 ng/ml) and C6 glioma cell CM, (50-fold concentrated) supported survival over the 4-day culture period of all the chromaffin cells present in culture 2 h after seeding. NGF (50 ng/ml) and the non-concentrated CMs from primary Schwann cell and astrocytes as well as Schwannoma and C6 glioma cell cultures, achieved the maintenance of only about half the number of cells above the baseline survival as compared to CNTF and the concentrated C6-CM. These results are compatible with two subsets of D8 chromaffin cells, one only supported by CNTF and the concentrated CM and the other supported by either NGF or CNTF. Either NGF or CNTF elicited neurite outgrowth from 15-20% of the surviving cells. Combination of maximal doses of NGF and CNTF caused a small increase in neurite recruitment beyond that elicited by either factor alone. Low doses of CNTF added to the effect of NGF, shifting the NGF titration curve by about 4-fold. Neurite outgrowth was also induced by the concentrated, but not the unconcentrated C6-CM. Laminin, fibronectin and PNPF did not affect the fibronectin and PNPF did not affect the recruitment of neurites as compared to a polyornithine substratum unless the cultures were supplemented with a neuronotrophic factor and carried for 7 days. However, even before showing effects on neurite recruitment these substrata affected various neuritic performances, such as length, neurite numbers and endings per cell.
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PMID:Neuronotrophic and neurite-promoting factors: effects on early postnatal chromaffin cells from rat adrenal medulla. 398 81

The extracellular matrix is involved in many aspects of tumor cell biology, including tumor invasion and metastasis. 2A6 and 81C6 are murine monoclonal antibodies that identify glioma-mesenchymal extracellular matrix antigens. The 81C6 antigen is a high molecular weight glycoprotein composed of Mr 230,000 subunits. The expression of 2A6 antigen, 81C6 glycoprotein, fibronectin (FN), and laminin (LN) was examined immunohistochemically in ten malignant gliomas (MG) and four medulloblastomas (MBT). 2A6 and 81C6 were expressed in similar patterns by the neoplastic neuroepithelial cells in 9/10 MG and 1/4 MBT. The staining was typically diffuse and amorphous, without visualization of distinct cell bodies or processes. Less frequently, antigen was detected within tumor cell cytoplasm. In most tumors the staining was greatest in the perivascular regions. In two MG, 2A6 and 81C6 were expressed only by a subpopulation of neoplastic cells. Although intense staining was also associated with hyperplastic vascular and mesenchymal cells, many small and medium size blood vessels stained weakly or not at all. In contrast, FN and LN were expressed uniformly and intensely in the tumor vasculature, but were not expressed by neoplastic neuroepithelial cells. The 2A6 antigen and 81C6 glycoprotein are immunohistochemically distinct from FN and LN. These monoclonal antibody-defined antigens are heterogeneously expressed by neoplastic neuroepithelial cells and hyperplastic vascular-mesenchymal elements in MG and MBT. The 2A6 and 81C6 monoclonal antibodies will be useful reagents in the investigation of the extracellular matrix of malignant neuroepithelial neoplasms.
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PMID:Immunolocalization of monoclonal antibody-defined extracellular matrix antigens in human brain tumors. 403 75

A novel human glioma-associated extracellular matrix (ECM) glycoprotein has been identified by murine monoclonal antibody 81C6. The glycoprotein, designated GMEM, is expressed in the ECM of glioma and mesenchymal cell cultures, in the perivascular matrix of endothelial proliferations of human gliomas, and in the stroma of human glioma xenografts in athymic mice, where it has been used as a target antigen for monoclonal antibody tumor localization and radioimaging. We report here on the immunochemical and biochemical characterization of GMEM. Polyacrylamide gel analysis of immunoprecipitated [3H]-leucine- and [3H]-glucosamine-labeled ECM from the human glioma cell line U-251MG has shown that GMEM is a high-molecular-weight macromolecule (Mr approximately 1,000,000) composed of Mr approximately 230,000 disulfide-bonded glycoprotein subunits. Immunoprecipitation, immunoblot, and one-dimensional peptide map analysis have shown that GMEM is distinct from human fibroblast and plasma fibronectin. These results support previous immunohistology and absorption analysis findings, indicating that GMEM is distinct from fibronectin, laminin, and glycosaminoglycans secreted by U-251MG.
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PMID:Immunochemical and biochemical characterization of a glioma-associated extracellular matrix glycoprotein. 406 74

Malignant gliomas constitute a morphologically diverse group of neoplasms that respond poorly to therapy. The median survival of patients with glioblastoma multiforme, the most common malignant glioma, is only 11 months. Several factors influence the therapeutic resistance of malignant gliomas, including tumor heterogeneity, local invasion, and non-uniform vascular permeability to therapeutic agents. Malignant gliomas vary in their expression of specific marker proteins such as glial fibrillary acidic protein and fibronectin, in their expression of specific cell surface antigens, in their in vitro growth properties and tumorigenicity in athymic nude mice, and in their chromosomal composition and DNA content. This biochemical, immunochemical, biologic, and chromosomal heterogeneity is observed between different gliomas and within individual gliomas both in vivo and in vitro. Marked vascular hyperplasia, a characteristic feature of malignant gliomas, is induced by growth factors that may stimulate not only vascular cells but also glioma cells. There is also heterogeneity in the ultrastructure and the permeability of glioma blood vessels. In animal brain tumor models, vascular permeability varies not only between different models but between different tumors and between different areas of a single tumor. An understanding of the cell biology of malignant gliomas may identify the factors that determine therapeutic resistance and provide strategies to overcome these factors.
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PMID:The biology of malignant gliomas--a comprehensive survey. 620 6

A serum-free defined medium has been formulated that supports proliferation and morphologic differentiation of U-251 MGsp human and C6-2BD rat glioma cells. This defined medium consists of a basal medium supplemented with transferrin, fibroblast growth factor, hydrocortisone, selenium, biotin, and fibronectin (G2 medium). When U-251 cells were plated in G2 medium on poly-D-lysine precoated dishes, their growth rate was 77% and final cell density was 82% of serum-grown counterparts. The growth rate of C6 cells in G2 medium was 67% compared to cells cultured in serum supplemented medium. Although G2 medium supported the growth of human and rat glioma cells, LA-N-1 human neuroblastoma and WI-38 human fibroblast cells showed no increase in cell number when grown in G2 medium compared to basal medium. A similar formulation (G3 medium), lacking fibroblast growth factor and hydrocortisone, supported the proliferation of RN-22 rat schwannoma cells. Morphologic differences were observed between cells grown in the presence of serum and in defined media. All three glial cell lines changed from a flattened shape in serum supplemented medium to a more spherical appearance in defined medium. In addition, both U-251 and C6 cells developed numerous processes, some reaching several cell diameters in length. These defined media will facilitate studies of the growth and differentiation of glial-derived cells.
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PMID:Proliferation of glial-derived cells in defined media. 621 93

Immunofluorescent stains for fibronectin (FN) and glial fibrillary acidic protein (GFAP) were used in conjunction with routine histologic stains to study tumors induced in squirrel and owl monkeys by JC virus from progressive multifocal leukoencephalopathy (PML). Three varieties of glioma were identified. The first and most common variety was a neoplasm similar to grade 4 astrocytoma in humans. The second had thin, normal-appearing FN-positive vessel walls and a vastly expanded neuroectodermal parenchyma which could not be characterized by routine histologic stains. Anti-GFAP revealed the glial nature of the parenchyma. Isolating glial parenchymal cells from divergent FN-positive cells has become important to neurooncology. This type of tumor may be of particular interest for such isolations due to its high ratio of glial cells to divergent cells. The third variety was not a homogeneous neoplasm. It occurred as focal regions within tumors of the first type, and consisted of giant cells with huge nuclei. These cells resemble the cells of a human giant cell glioblastoma and bear a slight similarity to the bizarre glial cells seen in PML. The rare human giant cell glioblastoma might have an association with JC virus or with PML.
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PMID:Glial and divergent cells in primate central nervous system tumors induced by JC virus isolated from human progressive multifocal leukoencephalopathy (PML). 630 61

The effect of several basement membrane components on the aggregation of acetylcholine (ACh) receptors on cultured myotubes was studied. Cultures were incubated for 16 to 24 hr with laminin, a heparan sulfate proteoglycan, collagen types IV and V, or fibronectin, alone, or together with medium conditioned by NG108-15 neuroblastoma X glioma hybrid cells (NCM). The number of ACh receptor aggregates per myotube was assayed by fluorescence microscopy of cultures stained with tetramethylrhodamine-labeled alpha-bungarotoxin. Laminin induced ACh receptor aggregation on primary rat myotubes and on myotubes formed by G8-1 clonal rat muscle cells. Laminin enhanced the receptor-aggregating activity of NCM in a concentration-dependent manner (0.6 to 6.0 micrograms/ml) and the number of aggregates formed in the presence of laminin and NCM together was greater than the sum of the aggregates induced by NCM and laminin separately. The aggregation factor in NCM is probably not laminin, since less than 10 ng/ml of laminin-like immunoreactivity was detected in NCM, and antiserum against laminin blocked the effects of laminin but had little effect on NCM aggregation activity. Collagen type V enhanced the receptor aggregation activity of NCM, but less strongly than laminin, and had little or no effect by itself. The other basement membrane components did not induce receptor aggregation or enhance the effect of NCM. Experiments in which ACh receptors were labeled before exposure of cultures to NCM and laminin indicated that laminin enhanced the rearrangement of receptors at the cell surface. Immunofluorescence microscopy indicated that laminin binds to the myotubes within 30 min and forms patches on the cell surface over a period of hours. Laminin bound to the myotube surface enhanced receptor aggregation as well as laminin continuously present in the culture medium. The results suggest the possibility that laminin could enhance the receptor aggregation activity of a neuronal factor(s) released at the developing neuromuscular junction.
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PMID:Laminin induces acetylcholine receptor aggregation on cultured myotubes and enhances the receptor aggregation activity of a neuronal factor. 634 13

The distribution and localization of a glioma-associated antigen defined by monoclonal antibody 81C6 has been examined using human cultured cell lines and tissues. Monoclonal antibody 81C6 was selected from a hybridoma fusion of spleen cells of mice immunized with the glial fibrillary acidic protein-positive human glioma cell line U-251 MG. Results of cell surface radioimmunoassay and absorption analysis demonstrated that 81C6 defined a glioma-mesenchymal extracellular matrix (GMEM) antigen expressed by 14 of 16 gliomas, 1 of 3 neuroblastomas, 1 of 7 melanomas, 2 of 6 sarcoma cell lines, and 8 of 9 cultured fibroblast lines. GMEM was not expressed by carcinoma or by the myeloid-lymphoid cell lines examined. Within the central nervous system, GMEM was expressed in 10 of 11 glioblastomas but was undetected in 5 of 6 astrocytomas and in normal adult and fetal brain by peroxidase-antiperoxidase immunohistology. In glioblastomas, the GMEM antigen was localized to basement membranes of the distinctive glomeruloid endothelial proliferations and hyperplastic blood vessels. The GMEM antigen was also expressed in 3 of 3 glioblastoma cell lines and 6 of 8 glioblastoma biopsy xenografts in athymic nude mice. Among non-central nervous system tissues and tumors, GMEM was found by peroxidase-antiperoxidase immunohistology in normal liver sinusoids, spleen red pulp sinusoids, kidney medullary tubule interstitium, and glomerular mesangium and in association with vascular and stromal elements of several undifferentiated tumors. The GMEM antigen is distinct from previously described forms of fibronectin, laminin, collagen types I to V, hyaluronic acid, chondroitin sulfate, and heparin, as determined by absorption analysis and immunohistological localization in tissues. The expression of GMEM in glioblastoma but not normal brain, association with glioblastoma-proliferative endothelium basement membranes, and expression in glioblastoma cell lines and nude mouse xenografts suggest that GMEM may be a useful marker of gliomas in vivo and in vitro.
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PMID:Human glioma-mesenchymal extracellular matrix antigen defined by monoclonal antibody. 634 60

Multicellular spheroids of a human glioma cell line (U-118 MG) and a human thyroid cancer cell line ( HTh -7) were analyzed for the presence of extracellular matrix (ECM) using light microscopy, transmission electron microscopy, and indirect immunofluorescence staining for fibronectin, laminin, and collagen. These studies were supplemented by analyses of glycosaminoglycans using autoradiography or chemical methods after metabolic labeling with [35S]sulfate or [3H]glucosamine in conjunction with various extraction procedures. The results showed that both types of spheroids contained an ECM composed of fibronectin, laminin, collagen, and glycosaminoglycans. The organization of the ECM in the spheroids seemed to be similar to that of tumors in vivo. These findings help justify the use of the spheroid system as an in vitro model for the study of biological phenomena of human tumors in vivo. Furthermore, it is concluded that the formation of an ECM in vitro is not confined to normal cells but can be promoted in transformed cells using appropriate culture conditions.
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PMID:Demonstration of an extracellular matrix in multicellular tumor spheroids. 637 2

The differential adhesion of cultured mammalian clonal cell lines to components of the extracellular matrix was examined by kinetic adhesion and long-term growth assays. Uniform artificial matrices were prepared by air drying collagen Type I solution (C) onto a microtiter well and then air drying a solution containing a single glycosaminoglycan (GAG): hyaluronic acid (HA), chondroitin sulfate-4 (CHS-4), or chondroitin sulfate-6 (CHS-6). The adhesion of [3H]thymidine-prelabeled cells suspended in fibronectin (FN) depleted medium was measured at 2 and 6 hr. Neuroblastoma (N18, Lan 1) and melanoma (B16, G361, S91) cell lines exhibited a significantly greater percentage of cells adhering to one or more C-GAG matrices compared with C matrices. Maximal adhesion at 2 hr was to C-HA. In contrast at 2 hr, two glial, two epithelial, and one fibroblastic cell line showed unchanged or significantly decreased binding to C-GAG compared with C matrices. Further experiments using a neuroblastoma (N18) and a glioma (C6) cell line indicated that the adhesion patterns were not altered either by the method of dissociation from the tissue culture dish, preincubation with exogenous GAG, or the addition of exogenous fibronectin. Assays of N18 and C6 adhesion to matrices made from a non-GAG polyanionic compound, polygalacturonic acid (PGA), did not yield the same adhesion patterns as C-HA matrices. Long-term growth studies of a neuroblastoma (N18) melanoma (S91), and glioma (C6) cell line on nonuniform matrices deliberately prepared with GAG-rich and GAG-poor regions complemented the observations from the kinetic adhesion assays. N18 and S91 cells did not grow on areas which did not contain GAG by toluidine blue staining. However, the C6 cells did not grow on areas which did strongly stain for GAG. A quantitative analysis of the long term growth of N18 and C6 cells substantiated these observations. All these data indicate that the cellular phenotype may be correlated with matrix adhesion. Neuroblastomas and melanomas have a greater affinity for GAG-containing matrices while glial, epithelial, and fibroblastic cells appear to have a greater or equal affinity for collagen matrices.
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PMID:Correlation of the cell phenotype of cultured cell lines with their adhesion to components of the extracellular matrix. 640 96


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