Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0017638 (
glioma
)
30,880
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
To evaluate the hypothesis that co-implantation of different rodent
glioma
cell lines might result in experimental brain tumours that more closely resemble human gliomas the neuropathology and immunocytochemical features of implantation gliomas derived from single cell lines (C6, A15A5, F98), two cell lines admixed 50:50 prior to implantation (C6 + F98 and C6 + A15A5) and three cell lines equally admixed (C6 + A15A5 + F98) was studied in the adult Wistar rat. Tumours grew consistently following implantation of the single and the two admixed cell lines, however tumour growth following triple mix implantation was considerably and consistently impaired. The tumours derived from admixed cell lines showed regional heterogeneity with areas characteristic of both the primary cell lines. Foci of lymphocytic infiltrates, tumoural necrosis, often with pseudopallisading, and peritumoural edema were consistent features of all tumours. Limited parenchymal and more extensive perivascular tumoural invasion was seen predominantly in tumours containing the C6 cell line. There were no significant differences in GFAP,
vimentin
and HSP70 staining between the mixed tumours, although the pure F98 and A15A5 tumours were, unlike the pure C6 gliomas, S-100 negative. Using PCNA expression as a measure of the tumour proliferation all except the tumours derived from the three cell lines mix, which had a staining index of 7-10%, had focal staining indices in viable tumour of between 40-80%. There was focal positive staining in both perilesional brain and in regions of all tumours for the macrophage markers ED-1 and ED-2. None of the three cell lines stained in vitro for either ED1 and ED2 but all were constitutively positive in vitro for OX-6, a proposed marker for antigen presenting cells. The macrophage and lymphocytic response suggest a vigorous but largely ineffective immunological response had been mounted against all tumours. The consistent failure of the triple mix tumours to grow is unexplained. This work has shown the feasibility of producing 'mixed' cell line experimental gliomas by combining two cell lines at the time of innoculation. However, the relative failure to produce (i) mixed tumours that have properties not inherent to either parent cell line and (ii) implantation
glioma
with three cell lines suggest there are limits to this approach. Admixture of cell lines at the time of implantation therefore does not make experimental
glioma
models that more closely resemble natural gliomas, and also has some particular disadvantages. This experimental approach is therefore not recommended for use in the study of tumour biology and in evaluating the effectiveness of novel therapies.
...
PMID:Can experimental models of rodent implantation glioma be improved? A study of pure and mixed glioma cell line tumours. 952 1
Whole mount electron microscopy of extracted cells combined with immunogold labeling techniques can be used to characterize the cytoskeletal architecture of cultured cells. As shown with subclones of the C6 rat
glioma
cell line, heavy metal shadowing was suitable for getting basic information concerning the arrangement of the various filament types within the networks. Pure carbon shadowing combined with immunogold double labeling proved to be optimal to identify linkages between filaments, to localize filament associated proteins and to follow the arrangement of filaments in dense arrays such as lamellipodiae and cell margins. Thin connecting filaments which interact with actin as well as with
vimentin
filaments and can be labeled with antibodies to the intermediate filament associated protein plectin may play a major role in the structural organization of the cytoskeleton of these cells.
...
PMID:Cytoskeleton architecture of C6 rat glioma cell subclones whole mount electron microscopy and immunogold labeling. 960 47
The establishment and characterization of two permanent
glioma
cell lines (8-MG-BA and 42-MG-BA) are described. Both cell lines were derived from the human glioblastoma multiforme. Analyzed cells were within the passage 200 to 220. The cells in both cultures showed similar morphology. In majority they consisted from flat polygonal cells. Growth kinetic studies demonstrated a population doubling time of 20 to 24 h in cell line 8-MG-BA and 48 to 54 h in cell line 42-MG-BA. The cell lines showed different hyperdiploid karyotypes. The immunofluorescence staining was performed for glial fibrillary acidic protein (GFAP) and
vimentin
. In the culture 8-MG-BA only a small amount of cells showed the GFAP-positive staining. At confluent 42-MG-BA culture the GFAP-positive cells reached 50 to 70% of all cells. Vimentin was found in all
glioma
cells in both cultures.
...
PMID:Characterization of two new permanent glioma cell lines 8-MG-BA and 42-MG-BA. 960 98
The identification of human brain tumor-associated markers could facilitate the development of new diagnostic and therapeutic strategies for these malignancies. The type III intermediate filament proteins (IFPs):
vimentin
, desmin and glial fibrillary acidic protein (GFAP) were studied in human
glioma
tissue extracts, in sera from
glioma
patients and in low passage
glioma
cell lines prepared from primary cultures of freshly dissected tumors. Radioimmunoassay (RIA) studies, using anti-GFAP, anti-desmin and anti-
vimentin
mAbs, showed high levels of these proteins in
glioma
extracts. Binding studies with authentic IFPs indicated the absence of circulating antibodies against these proteins in the sera of
glioma
patients. On the other hand, these sera showed high levels of
vimentin
. Binding studies with these antibodies using RIAs and western immunoblotting, showed that while anti-GFAF mAbs were specific to GFAP, anti-desmin mAb cross-reacted completely with GFAP, anti-
vimentin
mAb cross-reacted substantially with desmin and GFAP. Immunofluorescence staining of frozen sections revealed high levels of neurofilaments in gliomas and strikingly low levels in normal brain tissue. Double immunofluorescence staining showed co-occurrence of all three IFPs in the same filaments. This suggests either co-expression or cross-reactivity of these proteins due to their high degree of homology. Thus, caution should be exercised in the use and interpretation of immunohistochemical data using antibodies to IFs.
...
PMID:Human glioma associated intermediate filament proteins: over-expression, co-localization and cross-reactivity. 961 12
A comparison was made of rat primary astrocytes, C6
glioma
cells pre-treated with dibutyryl cyclic AMP, and the human astrocyte 132N1 cell line using a range of 40 compounds and the neutral red (NR) assay. The 40 chemicals included substances known to be toxic to astrocytes or neurons, to be generally cytotoxic or not thought to be toxic to nervous tissue. For those compounds which were toxic, changes in glial fibrillary acidic protein (GFAP) levels were measured in the primary and C6 cultures, and changes in
vimentin
and S-100 measured in the C6 cells. The number of compounds with EC50 values < 2000 microg/ml for the NR assay for the different cell cultures were as follows: primary astrocytes, 19; C6 cells, 15; and 1321N1 cells, 11. The log of the EC50 values for the NR assay for the test compounds between the three cell types was not significantly different at the 5% level by paired Student's t-test. For the toxic substances the correlation coefficients of the EC50 values between primary cells and the C6 or 1321N1 cells were r > 0.5, and between the C6 and 1321N1 cells r > 0.9. For GFAP there was a similar degree of correlation in EC50 values between the different cell types. The GFAP,
vimentin
and S-100 levels showed similar EC50 values for the toxicants, but were not as sensitive as the NR assay. The toxic substances caused altered morphology in the primary, C6 and 1321N1 cells, with increased branching of cell processes. The combined astrocyte systems identified 8 out of 9 substances reported to be toxic to astrocytes in vivo, together with substances which have general cytotoxic properties. A number of substances (including the 1 out of 9 reported gliotoxic substances), which may primarily affect neurons, which may affect nervous tissue after long-term exposure, or which are not thought to be toxic to nervous tissue, were not detected. The astrocyte systems positively identify gliotoxic and cytotoxic substances and will allow detailed mechanistic studies to be made on the different underlying mechanisms.
...
PMID:Evaluation of toxicity indicators in rat primary astrocytes, C6 glioma and human 1321N1 astrocytoma cells: can gliotoxicity be distinguished from cytotoxicity? 965 85
The temperature-sensitive mutant tsp53val135 accumulates in the cytoplasm of cells kept at the non-permissive temperature (39 degrees C), but is rapidly transported into the cell nucleus at the permissive temperature (30 degrees C). tsp53 thus may serve as a model for analysing cellular parameters influencing the subcellular location of p53. Here we provide evidence that retention of tsp53 in the cytoplasm at the non-permissive temperature is due to cytoskeletal anchorage of the p53 protein. Two sublines of C6 rat
glioma
cells differing in their expression of the intermediate filament protein
vimentin
(
vimentin
expressing or
vimentin
negative cells) were stably transfected with a vector encoding tsp53. Whereas cells of
vimentin
expressing C6 subclones retained tsp53 in the cytoplasm at the non-permissive temperature, cells of
vimentin
negative subclones exclusively harbored the tsp53 within their nuclei. Intermediate filament deficient cells that had been reconstituted with a full length
vimentin
protein again showed a cytoplasmic localization of tsp53, whereas in cells expressing a C-terminally truncated (tail-less)
vimentin
tsp53 localized to the nucleus. We conclude that cytoplasmic sequestration of tsp53 requires an intact intermediate filament system.
...
PMID:Cytoplasmic retention of mutant tsp53 is dependent on an intermediate filament protein (vimentin) scaffold. 969 50
Thyroid hormone (T3) is essential to normal brain development. Previously, we have shown that T3 induces cerebellar astrocyte proliferation. This effect is accompanied by alteration in glial fibrillary acidic protein (GFAP) and fibronectin organization. In the present study, we report that the C6
glioma
cell line, which expresses GFAP and is classified as an undifferentiated astrocytic cell type, is a target for T3 action. The C6 monolayers were treated with 50 nM T3 for 3 days, after which the cells were maintained for 2 days without medium changes. In C6 cells, T3 induced the expression of proteins of 107, 73 and 62 kDa. The hormone also up-regulated protein bands of 100 (+50%), 37 (+50%) and 25.5 kDa (+50%) and down-regulated proteins of 94 (-100%), 86.5 (-100%), 68 (-100%), 60 (-100%), 54 (-33%), 51 (-33%) and 43.5 kDa (-33%). We suggest, on the basis of molecular mass, that the 54-, 51- and 43.5-kDa proteins could be the cytoskeletal proteins
vimentin
, GFAP and actin, respectively. The down-regulation of these proteins may be involved in the effects of thyroid hormone on C6 differentiation.
...
PMID:Thyroid hormone regulates protein expression in C6 glioma cells. 987 99
In several neuropathological conditions, alphaB-crystallin and glial fibrillary acidic protein (GFAP) accumulate and form cytoplasmic inclusions in astrocytes. To explore the pathogenesis of the inclusions and the possible functions of the accumulated alphaB-crystallin, GFAP and alphaB-crystallin were overexpressed in cultured astrocytes by transient transfection. Human GFAP formed filamentous, cytoplasmic inclusions in mouse astrocytes, NIH3T3 cells, rat C6
glioma
cells, and human U251
glioma
cells. These human GFAP inclusions did not contain the endogenous
vimentin
or beta-tubulin, and the intermediate filament and microtubular networks of the transfected cells appeared normal. alphaB-crystallin and hsp25 were associated with the GFAP inclusions. Increasing intracellular alphaB-crystallin levels using recombinant adenoviruses, either before or after GFAP inclusions were formed, decreased the number of inclusion-bearing astrocytes and converted the human GFAP from an inclusion to a spread, filamentous form. These results suggest that alphaB-crystallin reorganizes abnormal intermediate filament aggregates into the normal filamentous network.
...
PMID:Formation of GFAP cytoplasmic inclusions in astrocytes and their disaggregation by alphaB-crystallin. 1032 8
Cytokines have roles in tumor biology and induce neurological manifestations. Cytokines produced in response to a brain tumor may generate neurological manifestations via paracrine action. We investigated cytokine modulation in an in vivo brain tumor model with behavioral, morphological, and molecular approaches. Rat C6
glioma
cells were implanted into the third cerebral ventricle of Wistar rats, their behavior was monitored, and the development of an intracranial tumor of astrocytic origin was confirmed by histology and positive immunostaining for
vimentin
, S-100 protein, and glial fibrillary acidic protein. Sensitive and specific RNase protection assays were used to analyze cytokine messenger RNA (mRNA) in brain regions from anorexic brain tumor-bearing animals. Brain tumor formation was associated with significant increased levels of interleukin (IL)-1beta, IL-1 receptor antagonist, IL-1 receptor type I, tumor necrosis factor (TNF)-alpha, and transforming growth factor (TGF)-beta1 mRNAs in the cerebellum, hippocampus, and hypothalamus. IL-1 receptor accessory proteins I and II mRNAs were increased in the cerebellum and hypothalamus. We also examined hypothalamic feeding-associated components: neuropeptide Y and proopiomelanocortin mRNAs were down-regulated, glycoprotein 130 mRNA levels were up-regulated, and leptin receptor (OB-R) mRNA levels were unchanged. These dissimilar profiles of mRNA expression suggest specificity of brain tumor-induced transcriptional changes. The data implicate cytokines as important factors in brain tumor-host interactions in vivo. The data also show that the C6 cell-induced
glioma
can be used as a behavioral-molecular model to study cytokine and neuropeptide modulation and action during the host biochemical and physiological responses to brain tumor development. Paracrine interactions seem pivotal because cytokine modulation was observed in various brain regions. These results also suggest that cytokine and neuropeptide changes during brain tumor progression are involved in brain tumor-associated neurological and neuropsychiatrical manifestations.
...
PMID:Brain tumor development in rats is associated with changes in central nervous system cytokine and neuropeptide systems. 1035 67
The term "chordoid glioma" was recently introduced to denote a circumscribed, apparently low-grade neoplasm arising in or preferentially involving the third ventricle of middle-aged women. We report biopsy and postmortem findings in a 60-year-old woman with symptoms of forgetfulness, headache, and lethargy. Neuroimaging showed a contrast-enhancing third ventricular mass with obstructive hydrocephalus. The tumor was subtotally resected. Microscopically, it consisted of clusters and strands of epithelioid cells in a mucoid matrix. Its margins were remarkably discrete and showed little tendency to infiltrate surrounding brain parenchyma. The majority of neoplastic cells were glial fibrillary acidic protein (GFAP) and
vimentin
positive, whereas S100 protein labeled only individual cells. Stains for epithelial membrane antigen (EMA) and cytokeratin were nonreactive. There was no evidence of neuroendocrine differentiation or expression of estrogen and progesteron receptors. Lymphoplasmacellular infiltrates were noted throughout the lesion and at the tumor-brain interface. The MIB-1 labeling index averaged 1.5%. At present, chordoid
glioma
is considered a glial neoplasm of uncertain histogenesis with distinct clinicopathologic features.
...
PMID:Chordoid glioma of the third ventricle: confirmatory report of a new entity. 1037 85
<< Previous
1
2
3
4
5
6
7
8
9
10
Next >>