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)

The effect of non-steroidal anti-inflammatory drugs (NSAIDs), acetylsalicylic acid (commonly known as aspirin), salicylic acid, piroxicam and indomethacin on the growth of rat glioma cells (RG 2) in vitro and aspirin in vivo was studied. The in vitro studies reveal that aspirin and salicylic acid strongly inhibit growth of rat glioma (RG 2) cells in concentrations used in medicine for treatment of rheumatic diseases. On the other hand, indomethacin and piroxicam had no effect, indicating that the inhibitory effect on tumor growth is not due to the inhibition of prostaglandin synthesis. The synthesis of ATP was markedly reduced (34% of control) in the presence of drugs, whereas protein synthesis measured as 3H-leucine incorporation was slightly more inhibited (73% of control) than cell growth. Aspirin administered to Fischer 344 rats inhibited growth of RG 2 cells inoculated into the caudate nucleus in vivo, both when administered the day before inoculation of tumor cells and when tumors had formed, i.e. 5 days post inoculation.
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PMID:Growth inhibition of rat glioma cells in vitro and in vivo by aspirin. 756 4

We have previously shown that diet restriction-induced depletion of large neutral amino acids (LNAAs) in murine plasma to 46% of control significantly enhances intracranial delivery of melphalan without enhancing delivery to other organs. Studies have now been conducted to determine whether more substantial LNAA depletion could further enhance intracranial delivery of melphalan. Treatment with L-amino acid oxidase (LOX) significantly depleted murine plasma LNAAs: phenylalanine, leucine, and tyrosine (> 95%); methionine (83%); isoleucine (70%); and valine (46%). Experiments evaluating the intracellular uptake of melphalan and high-pressure liquid chromatography quantitation of melphalan metabolites revealed, however, that melphalan is rapidly degraded in the presence of LOX, and that the timing of the administration of melphalan following the use of LOX to deplete LNAAs is crucial. Conditions were found under which LOX-mediated degradation of melphalan was minimized and LNAA depletion was maximized, resulting in a potentiation of the antitumor effect of melphalan on human glioma xenografts in nude mice. Such potentiation could not be obtained using diet restriction alone.
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PMID:The effect of L-amino acid oxidase on activity of melphalan against an intracranial xenograft. 763 79

A series of C-terminal linear endothelin analogues were prepared and their activities in C6 rat glioma cell line were tested. Among the synthetic analogues, IBDP 064, Fmoc-Leu-Asp-Ile-Ile-Trp-OH, was the most potent and selective inhibitor of endothelin-3-induced cell proliferation. Its action was comparable with that of the previously described peptide IRL 1038, [Cys11-Cys15]-ET-1(11-21), an ETB specific inhibitor.
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PMID:A new endothelin C-terminal analogue IBDP 064 antagonizes endothelin-3-induced cell proliferation. 765 97

Binding of plasmin(ogen) to rat C6 glioma cells is saturable and kringle-domain dependent. This interaction was studied as a model of plasmin(ogen) receptor interactions in nucleated mammalian cells. Apparent 125I-plasmin dissociation from C6 cell binding sites was slow; however, the dissociation rate was increased when the solution contained diisopropyl phosphoryl-plasmin (0.3 microM), fibrinogen (0.16 or 0.8 mg/ml), 1.08 mM D-Val-L-Leu-L-Lys-p-nitroanilide-HCl (S-2251), or epsilon-amino-n-caproic acid (EACA, 5.0 mM). EACA promoted the most rapid dissociation of plasmin. C6 cell-associated plasmin and plasmin in solution demonstrated similar amidase activity. Only specifically bound plasmin (75% of total binding) was active against S-2251. Plasmin that was initially bound to C6 cells digested fibrinogen in a time- and plasmin concentration-dependent manner. alpha 2-Antiplasmin (alpha 2AP, 0.1 microM) completely inhibited fibrinogenolysis by plasmin that was initially C6- or human umbilical vein endothelial-cell associated. Since alpha 2AP reacts selectively with plasmin in solution (minimally with plasmin bound to cells), fibrinogen digestion by cell-associated plasmin probably occurred only after the plasmin dissociated into solution. Crosslinked fibrin clots were formed in uniform layers over C6 cells. If the cells were incubated with plasmin before addition of fibrinogen and thrombin, the clots were rapidly lysed. alpha 2AP incompletely inhibited fibrinolysis when added after fibrin polymerization (44% inhibition with 0.1 microM alpha 2AP). Fibrinolysis was completely inhibited when alpha 2AP was added before fibrin polymerization. These studies suggest that plasmin must first dissociate from cellular binding sites to mediate fibrinogenolysis or fibrinolysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fibrinogenolytic and fibrinolytic activity of cell-associated plasmin. 767 97

A study was made of the effect of opioid peptides, (Leu)-enkephalin and its synthetic analog dalargin, on the maturation speed (differentiation) and proliferation activity of glioma C-6 cells. This effect on phenotypes of glioma C-6 cells was determined using some biochemical parameters: changes in the activity of glutamine synthetase (astrocytic marker) and cyclic nucleotide phosphorohydrolase (oligodendrocytic marker) in the culture of glioma C-6 cells in the early and late passages. The biochemical analysis was made at the Laboratory in Denver, USA, and we thank Prof. A. Vernadakis for the possibility to carry out a part of this work that helped us to find the growth activity of opioid peptides on the C-6 cells. Proliferation was examined in cultivation conditions approximately conforming the conditions of cultivation for the primary glial cell cultures. The control proliferation level was high in this case. It is demonstrated that opioid peptides accelerate (or strengthen) the expression of phenotypic signs in C-6 glioma cells in early and late passages changing specific activity of the marker enzymes, i.e. operating as a growth factor. Opioid peptides show glial growth factor characteristics on the glioma C-6 glial cell model as well, for glioma C-6 is known to be a perfect model to analyse the action of different substances on the glia.
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PMID:[The effect of opioid peptides on a decreased proliferation and on an increased maturation rate of glioma C-6 cells manifested by enhanced marker enzyme activity]. 770 17

It has already been reported that T cell infiltration is observed in brain tumor tissue but that general cellular immunity is suppressed in malignant brain tumor patients. In this report, the subsets of tumor infiltrating lymphocytes (TILs) and peripheral blood lymphocytes (PBLs) were analyzed in 8 patients with malignant glioma in order to investigate the relationship between the local and systemic immunological response in malignant brain tumor patients. TIL subsets in surgical specimens were analyzed immunohistochemically using the ABC method and monoclonal antibodies of the Leu series (anti-Leu 2a, 3a + b, 4 + 5b, 7, 12 and M5), and identified more precisely by double immunofluorescence staining (DIFS) using paired fluorescein isothiocyanate (FITC)-Leu 3a + b and phycoerythrin (PE)-Leu8 or FITC-Leu 2a and PE-Leu 15. PBL subsets were determined preoperatively by two-color analysis with a fluorescence-activated cell sorter (FACS) using fluorescence-labeled monoclonal antibodies (paired FITC-Leu 4 and PE-Leu 12, FITC-Leu 3a and PE-Leu 8, or FITC-Leu 2a and PE-Leu 15). Most TILs proved to be T lymphocytes containing Leu 3a + b+ (T helper/inducer) cells and Leu 2a+ (T suppressor/cytotoxic) cells in almost equal numbers, but there were too few TILs to kill the tumor cells. Detailed examination by DIFS revealed that 93% of the Leu 3a + b+ cells were helper T cells (Leu3a + b+.Leu8- cells) and that 88% of the Leu 2a+ cells were cytotoxic T cells (Leu 2a+.Leu15- cells). Analysis of PBLs showed statistically significant decreases in T cells as a whole and in helper T cells (Leu 3a+.Leu 8- cells).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Subset analysis of tumor infiltrating lymphocytes and peripheral blood lymphocytes in malignant glioma patients]. 778 23

Mutations in the p53 gene have been recognized in brain tumors, and clonal expansion of p53 mutant cells has been shown to be associated with glioma progression. However, studies on the p53 gene have been limited by the need for frozen tissues. We have developed a method utilizing polymerase chain reaction (PCR) for the direct analysis of p53 mutation by single-strand conformation polymorphism (SSCP) and by direct DNA sequencing of the p53 gene using a single 10-microns paraffin-embedded tissue section. We applied this method to screen for p53 gene mutations in exons 5-8 in human gliomas utilizing paraffin-embedded tissues. Twenty paraffin blocks containing tumor were selected from surgical specimens from 17 different adult patients. Tumors included six anaplastic astrocytomas (AAs), nine glioblastomas (GBs), and two mixed malignant gliomas (MMGs). The tissue section on the stained glass slide was used to guide microdissection of an unstained adjacent tissue section to ensure > 90% of the tumor cell population for p53 mutational analysis. Simultaneously, microdissection of the tissue was also carried out to obtain normal tissue from adjacent areas as a control. Mutations in the p53 gene were identified in 3 of 17 (18%) patients by PCR-SSCP analysis and subsequently confirmed by PCR-based DNA sequencing. Mutations in exon 5 resulting in amino acid substitution were found in one thalamic AA (codon 158, CGC > CTT: Arg > Leu) and one cerebral hemispheric GB (codon 151, CCG > CTG: Pro > Leu).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of p53 gene mutations in human gliomas by polymerase chain reaction-based single-strand conformation polymorphism and DNA sequencing. 816 51

Poly(A)+ RNA from C6-BU-1 rat glioma cells and rat astroglial cells induced isoleucine transport activity when injected into Xenopus laevis oocytes. The Na+-independent component of isoleucine transport was inhibited by leucine, phenylalanine and 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid (BCH) but neither by methylaminoisobutyric acid (MeAIB) nor lysine. A Km value of approx. 100 microM was determined for the Na+-independent transport of isoleucine. These data are in accordance with expression of a system L like transporter. By injection of size fractionated poly(A)+ RNA a length of approx. 1.9 kb was determined for the pertinent mRNA.
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PMID:Expression of Na+-independent isoleucine transport activity from rat brain in Xenopus laevis oocytes. 820 56

Anisoylated Lys-plasminogen streptokinase activator complex (APSAC) was purified from Eminase by chromatography on Superose-12. Purified APSAC did not significantly deacylate within 4 h at 4 degrees C in solution as determined by hydrolysis of D-Val-L-leu-L-lys-p-nitroanilide HCl (S-2251). At 37 degrees C, maximum amidase activity developed in 120 min; epsilon-amino-n-caproic acid (EACA) did not affect the apparent rate of APSAC deacylation but stabilized the streptokinase-plasmin(ogen) complex (SkPl) which formed. APSAC bound to C6 glioma cells and human umbilical vein endothelial cells (HUVECs) in culture. Binding as completely inhibited by EACA suggesting an essential role for the plasminogen kringle domains. Cell-associated APSAC deacylated to form active SkPl which hydrolyzed S-2251 and D-Val-Leu-Lys-7-amino-4-methyl coumarin. The rate of APSAC deacylation was increased when the APSAC was cell-associated. APSAC that was initially bound to C6 cells or HUVECs also activated 125I-plasminogen. This activity may have reflected cell-associated APSAC or APSAC but dissociated into solution. Plasmin was recovered bound to cells and in solution. These studies demonstrate that APSAC associates with cell-surfaces and retains activity. In the circulation, cell-surfaces may provide a significant pharmacologic compartment for intravenously administered APSAC.
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PMID:Binding of anisoylated Lys-plasminogen streptokinase activator complex to cells in culture. 838 80

We have succeeded in inducing progressive splenomegaly by inoculating 9L-glioma cells into the back subcutaneous regions of Fischer rats. The progressive splenomegaly was histologically characterized by progressively increased extramedullary haematopoiesis. Immunohistochemically Leu 7 positive cells were present in the enlarged spleen, suggesting that the spleen possessed natural killer (NK) cells. However, the splenic NK cell activity obtained in a 4h-51Cr release assay at 5 weeks after inoculation was below 5%, suggesting that the cytotoxic function of the NK cells was depressed. Bone marrow morphologically appeared not to be suppressed. Although the exact cause and mechanism of the progressive splenomegaly with prominent extramedullary haematopoiesis and severe suppression of the splenic NK cell activity remains speculative at present, it could be a unique manifestation of a systemic host-reaction reflected by the 9L-glioma continuously growing in the subcutaneous regions. This experiment could be a useful approach to the study of splenic and other reticuloendothelial roles in host-immunity in the tumour bearing state.
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PMID:Progressive splenomegaly with increasing extramedullary haematopoiesis in subcutaneous 9L-glioma bearing rats. 847 37


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