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

Human malignant glioma cells were cotransfected with an infectious molecular clone of the human immunodeficiency virus (HIV) and a selectable drug resistance gene (neo). HIV/neo-positive cell clones were maintained in continuous culture for over 5 months and showed the following characteristics: (i) expression of HIV antigens as detected by indirect immunofluorescence staining in 80-90% of cells; (ii) efficient production of HIV RNA and infectious progeny virus; (iii) minimal cytopathic effects (notably in cell morphology), in contrast to HIV-infected T lymphocytes. These results demonstrate that certain glial cells originating from human brain can support a chronic infection with HIV comparable to that observed in T lymphoid cell lines. The cell lines provide an in vitro model system for studies on the mechanism and biological effects of HIV infection in glial cells, and offer an alternative source of the virus that has not been Adapted to lymphocytes or macrophages.
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PMID:Establishment of human glial cell lines chronically infected with the human immunodeficiency virus. 333 39

Six isolates of the human immunodeficiency virus (HIV) showed differences in their ability to productively infect glioma-derived cell lines and early-passage human brain cell cultures. Susceptibility to HIV infection correlated well with the expression of the astrocyte marker glial fibrillary acidic protein. The CD4 molecule was expressed on some, but not all, of the brain-derived cells; however, no correlation was observed between CD4 protein expression and susceptibility to virus infection. The results show that HIV can productively infect human brain cells, particularly those of glial origin, and suggest that these cell types in the brain can harbor the virus.
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PMID:Human immunodeficiency virus can productively infect cultured human glial cells. 347 22

A malignant glioma cell line was infected with the human T-lymphotropic virus type IIIB isolate of the human immunodeficiency virus. Infection appeared to be latent rather than productive. Through contact with monocytic or lymphoid cells, the virus present in the glioma cells could be transmitted and gave rise to a fully productive infection.
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PMID:Infection of brain-derived cells with the human immunodeficiency virus. 364 20

Human immunodeficiency virus (HIV) is the causative agent of the acquired immune deficiency syndrome (AIDS). A large number of AIDS patients show evidence of neurologic involvement, known as AIDS-related subacute encephalopathy, which has been correlated with the presence of HIV in the brain. In this study, two genetically distinct but related viruses were isolated from one patient from two different sources in the central nervous system: brain tissue and cerebrospinal fluid. Both viruses were found to replicate in peripheral blood lymphocytes, but only virus from brain tissue will efficiently infect macrophage/monocytes. The viruses also differ in their ability to infect a brain glioma explant culture. This infection of the brain-derived cells in vitro is generally nonproductive, and appears to be some form of persistent or latent infection. These results indicate that genetic variation of HIV in vivo may result in altered cell tropisms and possibly implicate strains of HIV with glial cell tropism in the pathogenesis of some neurologic disorders of AIDS.
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PMID:Dual infection of the central nervous system by AIDS viruses with distinct cellular tropisms. 364 51

A patient who developed primary brain lymphoma 6 years following whole brain irradiation due to a low-grade glioma is described. The patient had no evidence of congenital or acquired immunodeficiency state and achieved a good and prompt response to aggressive chemotherapy, including high-dose methotrexate. The previous radiation therapy is implicated in the etiology of the lymphoma because of the geometric coincidence, the relatively long latency period and the different histology. A brief review of current literature is reported.
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PMID:Radiation-induced primary brain lymphoma: a case report. 757 Oct 30

Hypericin, a polycyclic aromatic dione isolated from plants, is presently being clinically evaluated as an antiviral agent in the treatment of human immunodeficiency virus (HIV) infection. In addition, it is known to be a potent protein kinase C inhibitor. To evaluate its potential as an inhibitor of glioma growth, an established (U87) and low-passage glioma line (93-492) were treated with hypericin in tissue culture for a period of 48 hours after passage. Hypericin inhibited the glioma growth in a dose-related manner, with a marked inhibition of growth in the low-micromolar concentration range (e.g., in line U87 and low-passage line 93-492, a concentration of hypericin of 10 mumol/L produced 62 and 76% decreases in [3H]thymidine uptake, respectively). Because the reported inhibitory effects of protein kinase C are enhanced by visible light, [3H]thymidine uptake was measured in both the presence and the absence of visible light. In glioma line A172, the presence of light slightly increased the inhibitory effect of hypericin. Moreover, an apoptosis (i.e., programmed cell death) assay was performed to determine whether the treatment of glioma cells with hypericin was cytostatic or cytocidal. Cells were harvested, and purified deoxyribonucleic acid (DNA) was analyzed by agarose gel electrophoresis. DNA from cells treated with hypericin for 48 hours exhibited a classical "ladder" pattern of oligonucleosome-sized fragments characteristic of apoptosis. These data suggest that the proven safe drug hypericin may have potential as an antiglioma agent; we suggest clinical trials.
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PMID:Hypericin: a potential antiglioma therapy. 780 14

Thirty-six lectins that recognize various sugar chains were examined for inhibitory activities against infection with human T-cell leukemia virus type I (HTLV-I). Wheat-germ agglutinin (WGA) was the most inhibitory among them: plating of the pseudotype of vesicular-stomatitis virus (VSV) bearing envelope antigens of HTLV-I was markedly inhibited by treatment of indicator cells with WGA just before adsorption, but not by treatment after virus adsorption. Treatment with WGA before adsorption, however, could not inhibit the plating of VSV, VSV pseudotypes of bovine leukemia virus, Moloney murine leukemia virus and human immunodeficiency virus type I. Syncytium formation induced by HTLV-I was also inhibited by WGA upon co-cultivation of U-251 MG human glioma cells or MOLT-4 human T-cells with HTLV-I-producing C91/PL cells. Formation of proviral DNA detected one day after infection was also inhibited when indicator cells had been treated with WGA before adsorption of HTLV-I, but not after its adsorption. These findings indicated that WGA specifically inhibits plating of HTLV-I when added to culture just before adsorption and suggested that a substance(s) containing sugar chains recognized by WGA might be involved in an adsorption step of HTLV-I.
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PMID:Inhibition of adsorption of human T-cell-leukemia virus type 1 by a plant lectin, wheat-germ agglutinin. 826 63

We examined transforming growth factor-beta (TGF-beta) activity in cerebrospinal fluid of 39 patients with various brain tumors, and found it in 10 glioma cases that had lesions related to subarachnoid space or ventricle. In one glioma case, TGF-beta detected on admission disappeared after radiation and chemotherapy. We confirmed that five glioma cell lines produced TGF-beta, and that four of them produced active form of TGF-beta directly. The active form of TGF-beta was also identified from cerebrospinal fluid before the acidification treatment in two cases. The calculated contents were 110 ng/ml and 18 ng/ml. These results indicate that active form of TGF-beta is directly produced by tumor cells in patients with glioma, and may contribute to immunodeficiency of the host.
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PMID:Detection of active form of transforming growth factor-beta in cerebrospinal fluid of patients with glioma. 832 Jan 72

The goal of our study was to assess whether the human immunodeficiency virus (HIV) coat protein gp120 induces functional alterations in astrocytes and microglia, known for their reactivity and involvement in most types of brain pathology. We hypothesized that gp120-induced anomalies in glial functions, if present, might be mediated by changes in the levels of intracellular messengers important for signal transduction, such as cAMP. Acute (10 min) exposure of cultured rat cortical astrocytes or microglia to 100 pM gp120 caused only a modest (50-60%), though statistically significant, elevation in cAMP levels, which was antagonized by the beta-adrenergic receptor antagonist propranolol. More importantly, the protein substantially depressed [by 30% (astrocytes) and 50% (microglia)] the large increase in cAMP induced by the beta-adrenergic agonist isoproterenol (10 nM), without affecting that induced by direct adenylate cyclase stimulation by forskolin. Qualitatively similar results were obtained using a glial fibrillary acidic protein (GFAP)-positive human glioma cell line. The depression of the beta-adrenergic response had functional consequences in both astrocytes and microglia. In astrocytes we studied the phosphorylation of the two major cytoskeletal proteins, vimentin and GFAP, which is normally stimulated by isoproterenol, and found that gp120 partially (40-50%) prevented such stimulation. In microglial cells, which are the major producers of inflammatory cytokines within the brain, gp120 partially antagonized the negative beta-adrenergic modulation of lipopolysaccharide (10 ng/ml)-induced production of tumor necrosis factor alpha. Our results suggest that, by interfering with the beta-adrenergic regulation of astrocytes and microglia, gp120 may alter astroglial "reactivity" and upset the delicate cytokine network responsible for the defense against viral and opportunistic infections.
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PMID:Human immunodeficiency virus coat protein gp120 inhibits the beta-adrenergic regulation of astroglial and microglial functions. 838 71

A 7-year and 11 month-old girl with cerebellar astrocytoma linked to familial ataxia-telangiectasia (AT) is presented. She was born as the 7th girl of a woman with aortic arch syndrome. Two elder sisters of the patient have ataxia telangiectasia. She had immunodeficiency, and cerebellar ataxia, but had no oculocutaneous telangiectasia. The risk of cancer developing in AT patients is about 1,200 times greater than that in age-matched controls. With regard to central nervous system tumours, seven primary tumours have been reported, such as 3 cases of medulloblastoma and 4 cases of glioma. Members of AT families who were under the age of 45 had a risk of dying of a malignant neoplasm five times greater than in the general population. However, there were no reports of glioma in AT families. In this case, it is suggested that IgA deficiency linked to familial AT may have contributed to the development of astrocytoma.
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PMID:Astrocytoma linked to familial ataxia-telangiectasia. 874 98


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