Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Radiolabeled GA-17, a murine monoclonal antibody that reacts specifically with glioma cells, bound to a small-cell lung cancer (SCLC) cell line NCI-H69 derived from neural cells, both in vitro and in vivo. The affinity constant of GA-17 F (ab')2 fragment binding to NCI-H69 was 1.02 x 10(8)/M while that to the glioma cell line U87MG was 1.22 x 10(8)/M. Iodine-125-labeled GA-17 F(ab')2 fragments injected i.v. localized well in NCI-H69 cells xenografted in nude mice. The percentage of the injected dose per gram accumulated in the xenografted tumor was 6.87 +/- 1.34% g-1 (mean +/- SD, n = 5) 24 h after injection. On the other hand, control monoclonal F(ab')2 fragments accumulated in the xenografted tumor at 0.75 +/- 0.30% g-1. The tumor-to-blood ratio was 1.8 for NCI-H69, while that of control F(ab')2 was 0.60. In conclusion, the radiolabeled GA-17 F(ab')2 fragment is expected to be useful clinically to visualize the small-cell lung cancer and in radioimmunotherapy.
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PMID:Scintigraphic detection of neural-cell-derived small-cell lung cancer using glioma-specific antibody. 812 56

Lactacidosis occurring in cerebral ischemia or trauma is a major mechanism of cytotoxic brain edema and brain damage. Respective effects of lactacidosis were currently analyzed in vitro by employment of the murine neuronal cell line, Neuro-2A, in order to obtain a better understanding of specific mechanisms underlying cell swelling and cell death in comparison with glial cells. The cells were suspended in a physiological medium in the presence of lactic acid at increasing concentrations. Levels of acidosis reaching from pH 6.8-5.6 were obtained while other parameters, such as osmolarity and electrolyte concentrations, were maintained in the physiological range. Assessment of cell swelling and cell viability using exclusion of propidium iodide was made by flow cytometry with employment of an advanced Coulter system. Swelling of Neuro-2A cells commenced once the pH in the medium was lowered to 6.8 or below. From this level downward, cell swelling was a function of the severity of acidosis and duration of exposure. For example, lactacidosis of pH 6.8 or 5.6 lasting 90 min led to an increase in cell volume to 109.5% or 159.6% of normal, respectively. Viability of the neuronal cells was 85% under control conditions. It remained in this range down to pH 6.2. At pH 5.6, however, cell viability decreased in a time-dependent fashion. At 90 min, only 48.9% of the neuronal cells were viable at pH 5.6. The swelling response and impairment of viability of the neuronal cells was compared with that of C6 glioma cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Swelling and death of neuronal cells by lactic acid. 824 14

Iodine-131-iododeoxyuridine (IUdR) uptake and retention was measured in two C6 glioma cell lines (C6m and C6a) with different growth characteristics. Animals with intracerebral (i.c.) C6a tumors had a mean survival of 16 days, whereas only 1 of 20 animals with i.c. C6m tumors died during an 8-wk period of observation. The growth of i.c. C6m tumors could be described by the Gompertz equation; tumor doubling time increased from 1.9 to 5.2 days between Days 8 and 16 after tumor inoculation. Corresponding measurements of 131I-IUdR uptake and retention (24 hr after IUdR administration) by i.c. C6m tumors were also time-dependent and decreased from 0.075 to 0.027 to 0.011 %dose/g in 8-, 10- and 16-day-old tumors, respectively. Iodine-131-IUdR uptake in "rapidly growing" i.c. C6a tumors was substantially higher (0.30 %dose/g at 24 hr) than that in "slowly growing" i.c. C6m tumors and corresponded with differences in the survival data. Subcutaneous C6a tumors had comparable high uptake values (0.49 %dose/g at 24 hr), and 93% of total tumor radioactivity was recovered in DNA 24 hr after IUdR administration. Clearance of radioactivity was rapid in nonproliferative tissues; more than 80% of plasma radioactivity was cleared in 24 hr. Tumor-to-cortex radioactivity ratios ranged from 100/1 to 120/1 and 150/1 between 24, 48 and 96 hr after IUdR injection respectively. A "washout strategy," which reduces tissue background activity and increases specificity for PET and SPECT imaging of IUdR-DNA incorporation, is possible with longer-lived radioisotopes of iodine.
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PMID:Iododeoxyuridine uptake and retention as a measure of tumor growth. 831 94

We present a method to assess quantitatively the immunological characteristics of tumours using radiolabelled monoclonal antibody and positron emission tomography (PET) to improve dosimetry for radioimmunotherapy. This method is illustrated with a glioma patient who was injected with 96.2 MBq of iodine-124 labelled 3F8, a murine antibody (IgG3) specific against the ganglioside GD2. Serial PET scans and plasma samples were taken over 11 days. A three-compartment model was used to estimate the plasma to tumour transfer constant (K1), the tumour to plasma transfer constant k2, the association and dissociation constants (k3, k4) of antibody binding, and the binding potential. Tumour radioactivity peaked at 18 h at 0.0045% ID/g. The kinetic parameters were estimated to be: K1 = 0.048 ml h-1 g-1, k2 = 0.16 h-1, k3 = 0.03 h-1, k4 = 0.015 h-1 and BP = 2.25. Based on these kinetic parameters, the amount of tumour-bound radiolabelled monoclonal antibody was calculated. This method permits estimates of both macrodosimetry and microdosimetry at the cellular level based on in vivo non-invasive measurement.
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PMID:Development of a method to measure kinetics of radiolabelled monoclonal antibody in human tumour with applications to microdosimetry: positron emission tomography studies of iodine-124 labelled 3F8 monoclonal antibody in glioma. 851 59

Statin, a 57-kDa nuclear protein, has been recognized as a unique marker of quiescent (G0) cells; specific monoclonal antibodies (MoAb) against statin have been produced and used to label resting cells in tissue sections and in cultured cells. We present an improved method for the identification of G0 cells by dual-parameter flow cytometry of statin expression and DNA content. The appropriate technical conditions were set up by using resting and cycling human fibroblasts as a model cell system. Several fixatives proved to be suitable for the immunocytochemical detection of statin; among them, 70% ethanol was selected because this fixation procedure is suitable for DNA staining with intercalating dyes and is routinely used for the immunolabeling of proliferation markers (such as proliferating cell nuclear antigen [PCNA] and Ki-67) and of bromodeoxyuridine (BrdUrd) incorporation. Following cell permeabilization with detergent, exposure to the antistatin antibody (S-44), and indirect fluorescein isothiocyanate immunolabeling, cells were counterstained for DNA with propidium iodide and analyzed by dual-parameter flow cytometry. In cells from several animal sources (rat thymocytes and C6 glioma cells, mouse 3T3 cells, and human MCF-7 cells), under different experimental conditions, the expression of statin was found to correlate inversely with that of PCNA and Ki-67, and with the BrdUrd labeling index. In dual-parameter flow scattergrams, G0 (statin positive) cells can be discriminated from the potentially cycling (statin negative) G1 cells, i.e., within a cell fraction having the same DNA content. This approach can be envisaged as a powerful tool both for monitoring changes in the resting cell fraction and for investigating the process of G0-G1 transition in unperturbed and drug-treated cell populations.
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PMID:Identification of resting cells by dual-parameter flow cytometry of statin expression and DNA content. 860 30

We investigated whether 2-[18F]-fluoro-2-deoxy-d-glucose (FDG) and carbon-11 methionine are suitable tracers to monitor the effects of therapy for low-grade gliomas. Ten patients with low-grade glioma without previous treatment were studied with FDG positron emission tomography. Additionally, l-[methyl-11C]methionine uptake was measured in five subjects before and 1 year after computerized tomography (CT)-guided stereotactic and computer-assisted implantation of iodine-125 seeds. All scans were 3D-matched to CT, isodose volumes were determined, and changes in glucose metabolism and methionine uptake were evaluated in tumour and brain tissue as a function of radiation dose. After 1 year glucose metabolism was not significantly altered up to a radiation dose of 300 Gy, whereas methionine uptake showed a significant dose-dependent decrease. Higher rates of decline were found in tumours with high basal methionine incorporation activity before therapy. These data suggest that measurement of methionine uptake is more suitable than measurement of FDG uptake for monitoring therapeutic effects in low-grade gliomas.
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PMID:Glucose consumption and methionine uptake in low-grade gliomas after iodine-125 brachytherapy. 869 67

Using single-photon emission tomography (SPET), the radiopharmaceutical l-3-iodine-123-alpha-methyl tyrosine (IMT) has been applied to the imaging of amino acid transport into brain tumours. It was the aim of this study to investigate whether IMT SPET is capable of differentiating between high-grade gliomas, low-grade gliomas and non-neoplastic brain lesions. To this end, IMT uptake was determined in 53 patients using the triple-headed SPET camera MULTISPECT 3. Twenty-eight of these subjects suffered from high-grade gliomas (WHO grade III or IV), 12 from low-grade gliomas (WHO grade II), and 13 from non-neoplastic brain lesions, including lesions after effective therapy of a glioma (five cases), infarctions (four cases), inflammatory lesions (three cases) and traumatic haematoma (one case). IMT uptake was significantly higher in high-grade gliomas than in low-grade gliomas and non-neoplastic lesions. IMT uptake by low-grade gliomas was not significantly different from that by non-neoplastic lesions. Diagnostic sensitivity and specificity were 71% and 83% for differentiating high-grade from low-grade gliomas, 82% and 100% for distinguishing high-grade gliomas from non-neoplastic lesions, and 50% and 100% for discriminating low-grade gliomas from non-neoplastic lesions. Analogously to positron emission tomography with radioactively labelled amino acids and fluorine-18 deoxyglucose, IMT SPET may aid in differentiating high-grade gliomas from histologically benign brain tumours and non-neoplastic brain lesions; it is of only limited value in differentiating between non-neoplastic lesions and histologically benign brain tumours.
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PMID:Uptake of iodine-123-alpha-methyl tyrosine by gliomas and non-neoplastic brain lesions. 878 Nov 39

The effect of mouse interferon-alpha/beta (MuIFN-alpha/beta on growth/viability, cell cycle regulation, 5-lipoxygenase (5-LO) protein expression, leukotriene B4 (LTB4) biosynthesis and glial fibrillary acidic protein (GFAP) expression of mouse glioma (G-26) cells in vitro was studied. The G-26 cells were treated with 800 IU/ml of MuIFN-alpha/beta for 1, 2, 3 and 4 days. The growth and viability of glioma cells was evaluated by [3H]-thymidine incorporation and MTT (3(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazoliumbromi de) assay, resulted in a time dependent decrease in [3H]-thymidine incorporation into DNA and MTT formazan formation, respectively. The cell cycle regulation measured by flow cytometry with propidium iodide staining revealed that the cell multiplication cycle was slowed down due to accumulation of cell in S-phase of the cell cycle, leading to inhibition in G0/G1 phase of the cell cycle. The 5-LO protein expression (measured by Western immunoblot analysis) and LTB4 biosynthesis (measured by enzyme immunoassay) were found to be increased by 2 to 2.4 fold and several fold respectively on days 3 and 4 of MuIFN-alpha/beta treatment. The GFAP protein expression was also found to be increased at least by 3 fold on day 4 of the MuIFN-alpha/beta treatment. These results suggest that inhibition in growth and thereby slowing of the cell multiplication cycle of glioma cells has resulted in upregulation of GFAP expression and 5-LO pathway.
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PMID:Modulation of glioma cell growth and 5-lipoxygenase expression by interferon. 904 9

1. In C6 glioma cells exposed to chemical hypoxia a massive release of lactate dehydrogenase (LDH) occurred at 3 and 6 h, coupled with an increased number of propidium-iodide positive dead cells. 2. Extracellular Na+ removal, which activates the Na(+)-Ca2+ exchanger as a Na+ efflux pathway and prevents Na+ entrance, significantly reduced LDH release and the number of propidium iodide positive C6 cells. 3. During chemical hypoxia, in the presence of extracellular Na+ ions, a progressive increase of [Ca2+]i occurred; in the absence of extracellular Na+ ions [Ca2+]i was enhanced to a greater extent. 4. The blockade of the Na(+)-Ca2+ exchanger by the amiloride derivative 5-(N-4-chlorobenzyl)-2',4'-dimethylbenzamil (CB-DMB), lanthanum (La3+) and the Ca2+ chelator EGTA, completely reverted the protective effect exerted by the removal of Na+ ions on C6 glioma cells exposed to chemical hypoxia. 5. The inhibition of the Na(+)-Ca2+ antiporter enhanced chemical hypoxia-induced LDH release when C6 glioma cells were incubated in the presence of physiological concentrations of extracellular Na+ ions (145 mM), suggesting that the blockade of the Na(+)-Ca2+ antiporter during chemical hypoxia can lead to increased cell damage. 6. Collectively, these results suggest that activation of the Na(+)-Ca2+ exchanger protects C6 glioma cells exposed to chemical hypoxia, whereas its pharmacological blockade can exacerbate cellular injury.
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PMID:Pharmacological evidence that the activation of the Na(+)-Ca2+ exchanger protects C6 glioma cells during chemical hypoxia. 915 41

We have investigated the expression patterns and subcellular localization in nervous tissue of glypican, a major glycosylphosphatidylinositol-anchored heparan sulfate proteoglycan that is predominantly synthesized by neurons, and of biglycan, a small, leucine-rich chondroitin sulfate proteoglycan. By laser scanning confocal microscopy of rat central nervous tissue and C6 glioma cells, we found that a significant portion of the glypican and biglycan immunoreactivity colocalized with nuclear staining by propidium iodide and was also seen in isolated nuclei. In certain regions, staining was selective, insofar as glypican and biglycan immunoreactivity in the nucleus was seen predominantly in a subpopulation of large spinal cord neurons. The amino acid sequences of both proteoglycans contain potential nuclear localization signals, and these were demonstrated to be functional based on their ability to target beta-galactosidase fusion proteins to the nuclei of transfected 293 cells. Nuclear localization of glypican beta-galactosidase or Fc fusion proteins in transfected 293 cells and C6 glioma cells was greatly reduced or abolished after mutation of the basic amino acids or deletion of the sequence containing the nuclear localization signal, and no nuclear staining was seen in the case of heparan sulfate and chondroitin sulfate proteoglycans that do not possess a nuclear localization signal, such as syndecan-3 or decorin (which is closely related in structure to biglycan). Transfection of COS-1 cells with an epitope-tagged glypican cDNA demonstrated transport of the full-length proteoglycan to the nucleus, and there are also dynamic changes in the pattern of glypican immunoreactivity in the nucleus of C6 cells both during cell division and correlated with different phases of the cell cycle. Our data therefore suggest that in certain cells and central nervous system regions, glypican and biglycan may be involved in the regulation of cell division and survival by directly participating in nuclear processes.
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PMID:Glypican and biglycan in the nuclei of neurons and glioma cells: presence of functional nuclear localization signals and dynamic changes in glypican during the cell cycle. 936 4


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