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)

We have compared the rate and extent of adhesion of various types of mouse tumor cells to endothelial cells derived from different organ sources. Our panel of tumors has included sarcoma, bladder carcinoma, glioma, teratoma, hepatoma, endothelioma, mammary adenocarcinoma, and lymphoma cells. Endothelial cell monolayers have included murine microvascular endothelial cells from ovary, brain, lung, and liver as well as large vessel endothelium from thoracic duct and dorsal aorta. Tumor cells differ both in the adhesive propensity and adhesive preference for different endothelial cells. Some, but not all, of the adhesive preferences correlate with the known in vivo metastatic behavior of these tumors. Our results support the hypothesis that endothelial cell surface-associated specificities may play a significant role in determining the pattern of metastasis.
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PMID:Specificity of adhesion between murine tumor cells and capillary endothelium: an in vitro correlate of preferential metastasis in vivo. 381 50

The isomeric mixtures of platinum complexes of diaminocyclohexane (DACH) had been found active on several murine tumors. A recent separation of the oxalato-platinum complex of trans-l-DACH isomer allowed more precise screening studies and permitted the selection of one compound: l-OHP was submitted to our murine tumor screening system. The drug was given: (a) at doses of 1-12 mg/kg i.p. or i.v. on day 1, 5 and 9 compared to identical doses of cis-dichlorodiamine platinum II (CDDP) in L1210 bearing mice and (b) to AkR leukemia, LGC lymphoma, glioma 26, B16 melanoma, MA 16-C mammary carcinoma and Lewis lung carcinoma bearing mice at 2 dosages: 5 mg/kg (minimal effective dose on L1210), and 8 mg/kg (subtoxic dose in L1210). Acute LD10 and LD50 appeared similar to CDDP and l-OHP. l-OHP administered i.p. was more active on L1210 than CDDP. On L1210 grafted intracerebrally and on LGC lymphoma l-OHP increased significantly the lifespan while CDDP was inactive. On AkR leukemia, both drugs were active but l-OHP was less toxic. Both drugs were inactive on murine solid tumors. No renal toxicity was observed with l-OHP as compared to CDDP.
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PMID:Antitumor activity of l-OHP in mice. 403 73

Exposure of several mammalian cell lines to isoproterenol resulted in a desensitization of the beta-adrenergic receptor-adenylate cyclase system in membranes isolated from the cells. Under the experimental conditions chosen, desensitization was accompanied by a minimal loss of beta-receptors. The cells tested included HeLa, S49 cyc- lymphoma, and rat glioma C6. The functional activity of the beta-receptors was determined by coupling them to a foreign adenylate cyclase by membrane fusion. The donor membranes were treated to inactivate the regulatory and catalytic components of adenylate cyclase. The acceptor membranes were from Friend erythroleukemic cells (Fr cells), which lack beta-receptors, and HeLa cells treated overnight with isoproterenol to eliminate their receptors. The fused membranes were assayed for agonist-stimulated activity, which was always reduced when the donor beta-receptors were from the desensitized membranes. The desensitization appeared to be specific for beta-receptors, as the activity of other receptors and cyclase components was not altered. By fusing HeLa membranes with intact Fr cells, we directly measure the intrinsic activity of native and desensitized beta-receptors. For an equal amount of transferred beta-receptors, the activity was 40%-50% lower when the donor membranes were from desensitized cells. Our results clearly indicate that desensitization mediated by a beta-agonist in mammalian cells results in a functional alteration of the beta-receptor.
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PMID:Functional alteration of the beta-adrenergic receptor during desensitization of mammalian adenylate cyclase by beta-agonists. 609 12

Suppressor T cells in syngeneic tumor-bearing mice that inhibited in vitro generation of tumor antigen-specific cytotoxic T lymphocytes were characterized with respect to the kinetics, the nature and the target specificity, using murine malignant glioma (a methylcholanthrene-induced malignant ependymoblastoma, 203-glioma). Suppressor cell activity was assessed by the inhibition of tumor cell killing activity of cytotoxic T lymphocytes, which were prepared from splenic T enriched lymphocytes of mice immunized with 1 X 10(6) mitomycin C (50 micrograms/ml, 45 minutes)-treated 203-glioma cells twice at an interval of 7 days. It was confirmed that suppressor T cells were generated in 203-glioma-bearing mice, and they were tumor antigen-specific as evidenced by the fact that sensitized splenic T lymphocytes from mice bearing other syngeneic EL4 thymoma or allogeneic P 815 mastocytoma or YAC-1 T cell lymphoma did not exhibit the inhibition of the cytotoxic T lymphocyte activity against 203-glioma cells. Significant suppressor cell activity was detected in spleen cells 1 to 5 days after the subcutaneous inoculation of 203-glioma cells with the peak activity on day 3 and it disappeared as early as on day 7, suggesting strongly that the turn-over of suppressor T cells is very quick. Surface markers of suppressor T cells in 203-glioma-bearing mice were checked on day 3 with the results that the suppressor cell activity was eliminated by the treatment with anti-Lyt-2 monoclonal antibody and complement, indicating that the phenotype of suppressor T cells is Lyt-1-.2.3+.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Suppressor mechanism in tumor immunology: characteristics of suppressor T-cells in glioma-bearing mice]. 619 6

The incorporation of methionine, lysine, and leucine into protein was studied in Ca2+-depleted and Ca2+-restored preparations of C-6 glial tumor cells in minimal medium. Although incorporation proceeded at linear rates in both preparations for more than 1 h and into the same spectrum of proteins, Ca2+-restored cells incorporated amino acid 5- to 10-fold more rapidly than Ca2+-depleted cells. Addition of approximately 200 microM Ca2+ in excess of chelator was required to achieve maximal rates of incorporation in Ca2+-depleted preparations. Stimulation by Ca2+ was rapid in onset (several minutes) and slowly reversible by chelator. Ca2+ was uniquely potent and specific among physiologically occurring cations in conferring such stimulation. Stimulation of amino acid incorporation by Ca2+ occurred over a broad range of pH and osmolarities and was facilitated by Mg2+. The effects of Ca2+ in stimulating amino acid incorporation were not traceable to changes in cAMP metabolism, amino acid uptake, protein catabolism, cell ATP or GTP content, or aminoacylation of transfer RNA. Actinomycin D (1 microgram/ml) did not block the stimulatory effects of Ca2+ although puromycin and cycloheximide did. The stimulatory effects of Ca2+ on protein synthesis were not restricted to C-6 in minimal medium. Protein synthesis was reduced by ethylene glycol bis(B-aminoethyl ether)-N,N,N',N'-tetraacetic acid 40 to 75% in C-6 glioma, GH3 pituitary tumor, PC-12 adrenal tumor, N2A neuroblastoma, and HeLa cells incubated under simulated growth conditions with various enriched media and sera. Ca2+-depleted S49 lymphoma, CHO ovarian tumor, and normal, dispersed chicken embryo cells in enriched medium responded to Ca2+ restoration with increased rates of protein synthesis as did collagenase-dispersed normal rat liver cells in minimal medium. Protein synthesis in rabbit reticulocyte lysates was also inhibited by Ca2+-selective chelators or by Ca2+ removal by parvalbumin affinity chromatography and the inhibition was reversed by Ca2+. These findings are consistent with the existence of a Ca2+ requirement in the translational phase of protein synthesis in eukaryotic cells.
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PMID:Identification of a Ca2+ requirement for protein synthesis in eukaryotic cells. 631 27

The water soluble beta-adrenergic ligand [3H]CGP-12177 was used to measure the cell surface receptors in intact cells. In two cell lines, C6 glioma and WEHI 7 lymphoma cells, -50% of the cell surface receptors disappear within minutes of incubation of the cells with isoproterenol. The receptors can still be detected in homogenates and reappear on the cell surface when cells are washed and reincubated at 37 degrees C. The data agree with a disappearance of the receptors from the cell surface by an agonist-mediated endocytosis.
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PMID:Rapid and reversible disappearance of beta-adrenergic cell surface receptors. 632 54

Correct diagnosis of malignant lymphoma of the brain and differentiation from malignant glioma, metastases, meningeoma and infection is often difficult. With the aim of finding characteristics pointing to the correct diagnosis all CT examinations from 16 patients with primary or secondary lymphoma of the brain were analysed. In 3 of 10 patients with primary lymphoma and 4 of 6 with secondary lymphoma the tumors were multiple. No differences between the CT appearance of primary and secondary lymphoma were found except that secondary lymphomas were generally smaller and more often multiple. The lymphomas were most often well demarcated, had a density equal to or slightly higher than normal brain tissue, were surrounded by no or slight edema and showed a moderate to marked contrast enhancement. The tumors were situated in the basal ganglia, corpus callosum or cerebellum in high frequency and were always in contact with either the ependyma of the ventricles or the superficial subarachnoid space. A tumor with widespread infiltration of the surroundings of the ventricles seen in 6 patients in the material is highly characteristic of lymphoma.
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PMID:Computed tomography of malignant lymphoma of the brain. 637 16

A murine monoclonal antibody (monoclonal antibody 126) produced against cultured human neuroblastoma cells (LAN-1) was found to be specifically directed to a disialoganglioside (GD2) antigen preferentially expressed on both cell lines and tissues derived from melanoma and neuroblastoma. In enzyme-linked immunosorbent assays, monoclonal antibody 126 failed to react with leukemic and lymphoblastoid cells as well as with a variety of carcinoma and sarcoma cell lines. Immunohistological analysis by the immunoperoxidase technique revealed strong reactivity of monoclonal antibody 126 with frozen and formaldehyde-fixed neuroblastoma and melanoma tissues. Tissues from patients with glioma or with small cell cancer of the lung showed faint staining, whereas those from individuals with sarcoma, lymphoma, and a variety of other neoplasms proved to be negative. Sera of neuroblastoma patients showed significantly elevated GD2 levels compared to normal children (p less than 0.001) and children with other tumors (p less than 0.001) as determined by a quantitative competitive enzyme-linked immunosorbent assay. Furthermore, the GD2 serum level of one neuroblastoma patient, when followed serially, was found to correlate with progression of disease, suggesting the potential usefulness of this assay for the diagnosis and monitoring of neuroblastoma.
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PMID:Detection of ganglioside GD2 in tumor tissues and sera of neuroblastoma patients. 649 49

C.T. scans of 19 patients with histologically proved primary lymphoma of the brain were reviewed and divided into three groups: solitary tumors (58%), multifocal tumors (31,5%), diffuse involvement of the brain (10,5%). The C.T. differential diagnosis are manifold, including meningioma, glioma, metastases, progressive multifocal leukoencephalopathy. Arteriography is not specific, but, correlation with C.T. results may suggest the correct diagnosis and encourage biopsy. The radiosensitivity of primary lymphoma of the brain emphasizes, the importance of an early diagnosis.
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PMID:Computed tomography in primary lymphoma of the brain. 650 18

The cholinergic agonist carbachol, epinephrine, and the opiate morphine all inhibit prostaglandin E1 (PGE1)-stimulated adenylate cyclase in homogenates from the neuroblastoma-glioma hybrid NG108-15. Pretreatment of the hybrid with 100 microM carbachol resulted in the rapid loss (desensitization) of the carbachol inhibition of adenylate cyclase (t1/2 less than 3 min). The desensitization of the carbachol inhibition was blocked by 0.1 microM atropine. Pretreatment with carbachol (1-24 h) did not significantly affect the inhibition of adenylate cyclase by either epinephrine or morphine, nor did it alter the PGE1-stimulated activity, that is, no supersensitization was observed. Cholate extracts of the particulate fraction from either carbachol-desensitized or of control NG108-15 were able to reconstitute adenylate cyclase activities of the coupling proteins (G/F)-deficient cyc- lymphoma cell membranes with equal efficacy. These results suggested that the coupling proteins of the adenylate cyclase were not altered by the carbachol pretreatment and that desensitization occurs at the receptor or at a receptor-associated level. However, the possibility remained that specific domains of the G/F, which interact only with muscarinic receptors, were altered.
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PMID:Specific muscarinic-cholinergic desensitization in the neuroblastoma-glioma hybrid NG108-15. 688 29


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