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)

Between 1982 and 1988, 174 brains were systematically collected from consecutive, autopsied AIDS patients in a Parisian general hospital without neurology and psychiatry departments. The data obtained under these conditions provide reliable information on the frequency of central nervous system (CNS) involvement in a non-selected population of AIDS patients, most of whom were homosexuals (75.9%). One or several lesions were observed in 148 cases (85%). HIV encephalitis and/or leucoencephalopathy with multinucleated giant cells was found in 33 cases (18.9%). Opportunistic infections were identified in 91 patients (52.3%): toxoplasmosis (65 cases; 37.3%), cytomegalovirus encephalitis (25 cases; 14.3%), cryptococcosis (9 cases; 5.8%), progressive multifocal leukoencephalitis (5 cases; 2.8%), candidosis (1 case) and tuberculosis (1 case). Neoplasias were observed in 23 patients: primary (16 cases; 17.9%) or secondary malignant non Hodgkin's large B-cell lymphoma (3 cas; 1.1%), Kaposi's sarcoma (1 case) and glioma (3 cases; 1.1%). Non-specific lesions (vasculitic, hemorrhagic, metabolic and especially microglial nodules) were common. During the 6 years of study, the rate of CNS involvement was constant. The number of toxoplasmosis cases per year was stable, however, evolutive forms were more prevalent between 1982 and 1986, whereas treated inactive lesions were seen most frequently thereafter. The opportunistic complications were often associated and it should be noted that HIV encephalitis was associated with one of several such infections in 85% of the patients. This high rate of association suggests that these opportunistic infections may play a role in the pathogenesis of HIV encephalitis.
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PMID:[Neuropathology of the brain in 174 patients who died of AIDS in a Paris hospital 1982-1988]. 131 51

A new case of supratentorial malignant glioma is reported in an HIV-1 infected male homosexual. Tumours of the nervous system account for only 5 to 10 percent of neurological complications of AIDS, and most of them are lymphomas or metastases from Kaposi's sarcomas. In fact, HIV-1 is a neurotropic lentivirus, not transforming by definition. Our patient had a frontal tumoral syndrome resistant to the conventional anti-toxoplasmic treatment. Pathological examination of a tumoral fragment obtained by stereotactic biopsy showed that according to the WHO criteria the tumour was a glioblastoma. The mechanism through which HIV infection results in malignant transformation of astrocytes is conjectural. There is no consensus on whether the virus is located in glial cells, but the transgenic animal technique suggests that the tat gene might play a certain role. Other hypotheses concerning the indirect neurotoxicity of HIV have been put forward, notably that of viral coinfection with viruses of the papova group.
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PMID:[Cerebral glioblastoma: a new complication of HIV-1 infection]. 132 36

A 32-year-old homosexual man presented with headache and progressive right hemiparesis. CT scan revealed a heterogeneous ring-enhancing mass in the left parietooccipital lobe which proved to be astrocytoma. Clinicians should be aware of this new and unusual association of a cerebral glioma and acquired immune deficiency syndrome. Tissue examination is essential for proper diagnosis.
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PMID:Acquired immunodeficiency syndrome associated with cerebral astrocytoma. 154 79

Association of glioma with AIDS is unusual. Cytomegalovirus (CMV) infection of glioma has not been documented in AIDS or non-AIDS patients. We present the case of a 37-year-old homosexual, HIV positive man who had a history of pneumocystis pneumonia and died of disseminated CMV infection and an anaplastic astrocytoma (5 x 5 x 4 cm) of the left temporal lobe. Part of the tumor was severely infected by CMV as demonstrated by immunohistochemical stain. Intranuclear and intracytoplasmic CMV inclusions were present in the cytomegalic cells whose astrocytic nature was identified by immunostain for GFAP. CMV-bearing cells were scattered throughout the astrocytoma but were rarely seen outside the tumor. CMV-bearing endothelial cells were seen in several capillaries within the tumor. Microglial nodules were scattered within the tumor and some contained CMV-infected cells. Many multinucleated giant cells (MNGC) with circularly arranged small nuclei were present in the infected area of the tumor and some showed fusion with cytomegalic cells. MNGC were absent outside the tumor. CMV ependymitis was not seen. The findings suggest that a) astrocytoma cells are permissive to CMV infection, b) that they may be more susceptible to CMV infection and replication than normal brain tissue, and c) the hyperplastic endothelia and abnormal blood brain barrier of the astrocytoma may facilitate the entry of CMV itno the tumor.
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PMID:Cytomegalovirus infection of cerebral astrocytoma in an AIDS patient. 165 Mar 2

Interferons are currently the most widely used biological response modifiers. They are of high clinical value in haematological malignancies (chronic myelogenous leukaemia, multiple myeloma, non-Hodgkin lymphoma), in solid tumours (malignant melanoma, hypernephroma, pancreas neoplasms, carcinoid tumours, Kaposi's sarcoma, glioma, in ovarium, cervix and bladder carcinoma, and in basalioma) and in infectious diseases (chronic hepatitis B, chronic non-A/non-B hepatitis, chronic delta hepatitis, AIDS, Papova virus and Rhinovirus infections, leishmaniasis, leprosy) and some other conditions. Although the mechanism of action of interferons has not been explained in every detail these agents are promising therapeutic means in a number of diseases.
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PMID:Role of interferon in clinical practice. 172 32

Human promonocyte cells chronically infected with human immunodeficiency virus type (HIV-1) (clone U1.1.5) were grown in the presence of media conditioned by human astrocytes and glioma cell lines U251 and 253. HIV-1 expression was assessed by measuring reverse transcriptase activity. All media conditioned by unstimulated and lipopolysaccharide (LPS) stimulated glial cells induced HIV-1 expression and contained detectable levels of interleukin-6 (IL-6) but not tumor necrosis factor-alpha (TNF-alpha). An antibody against IL-6, but not against TNF-alpha, reduced the induction of HIV-1 by the conditioned media in a concentration-dependent manner. The magnitude of HIV-1 induction by the conditioned media was proportional to the concentration of IL-6 in them. The data indicate that normal and transformed human astrocytes are capable of stimulating HIV-1 expression in chronically infected promonocytic cells by secreting IL-6. The results demonstrate that cytokines secreted by neural cells could play an important role in regulating HIV-1 expression in the brain.
AIDS Res Hum Retroviruses 1991 Sep
PMID:Human astrocytes stimulate HIV-1 expression in a chronically infected promonocyte clone via interleukin-6. 174 78

A panel of nine monoclonal antibodies raised against human hemopoietic cells was used for immunohistological labeling of frozen sections of human nervous tissues and tumors. Three antibodies showed a remarkably consistent labeling pattern when tested on 18 samples of normal or reactive tissue, on 31 neurogenic and 17 non-neurogenic tumors in an indirect immunofluorescence technique. VIM C6, an antibody recognizing cells of the granulocyte series, showed surface labeling of normal and reactive glial cells and of all types of glioma regardless of the grade of malignancy. VIT 13, an antibody recognizing activated T-cells, labeled the processes of normal, reactive, and neoplastic glia in a manner very similar to but not identical with glial fibrillary acidic protein (GFAP). VIB C5, an antibody recognizing B cells and granulocytes, showed surface labeling restricted to malignant cells (malignant gliomas and primitive neuroectodermal tumors) and fetal brain, thus recognizing, within the nervous system, an oncofetal antigen. Due to this operational specificity within the nervous system, some of the antibodies described here might have a role as diagnostic markers for CNS tumors. This study confirms and expands previous data that sharing of antigenic determinants by hemopoietic cells and nervous tissue or neurogenic tumors is common. However, the significance of such cross-recognition is still obscure. It is tempting to speculate that cross-reacting auto-antibodies might contribute to tissue damage in some immune-mediated neurologic diseases (myasthenia gravis, multiple sclerosis, CNS involvement in systemic lupus erythematosus) or to impairment of immunoregulation in multiple sclerosis or glioma patients. Furthermore, sharing of surface determinants might be responsible for the dual tissue tropism of some viruses, including the lymphotrophic virus (HTLV) in the encephalopathy of the acquired immune deficiency syndrome (AIDS).
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PMID:Shared antigenic determinants between human hemopoietic cells and nervous tissues and tumors. 241 Oct 97

Dideoxycytidine (ddCyd), an inhibitor of AIDS-related HIV, has been examined for effects on cell proliferation and phosphatidylcholine synthesis in tumor lines of nervous system origin. Uptake and metabolism of [3H]ddCyd, observed in all cells, was greatest in one human neuroblastoma line, HTB-10. Growth of the HTB-10 line was markedly inhibited by 40 microM ddCyd, whereas growth of C6 glioma and N1E-115 or HTB-11 neuroblastoma cells was unaltered. Phosphatidylcholine synthesis in the presence or absence of stimulation by phorbol ester was not specifically altered by ddCyd. Thus, ddCyd was incorporated and inhibited growth in a cell-specific manner but had little effect on cytidine-dependent phospholipid synthesis. This suggests that some cells derived from the nervous system may be more susceptible than others with respect to the positive and negative effects of ddCyd as a potential antiviral drug.
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PMID:Dideoxycytidine, an anti-HIV drug, selectively inhibits growth but not phosphatidylcholine metabolism in neuroblastoma and glioma cells. 254 24

In this paper we present the results of post-mortem examinations of the central nervous system in 61 male patients who died with Acquired Immunodeficiency Syndrome (AIDS); it includes 23 patients with reported neurological abnormalities at the time of presentation. The analysis revealed central nervous system (CNS) neoplasms (lymphoma, Kaposi's sarcoma) and a variety of inflammatory lesions (bacterial, fungal, protozoal and viral) in 32 cases. A total of 11 patients without opportunistic infections showed significant brain abnormalities characterized by microglial nodules and/or multinucleated giant cells, changes which are probably related to infection by human immunodeficiency virus (HIV). In addition, we describes results from a series of experiments designed to define the target cell population of HIV in the brain. The expression of CD4 complex--putative receptor for HIV--was investigated using short-term cultured brain cells taken from embryonic brain anlage and from different regions of fetal brain; glioma cells were also used. Cells derived from normal embryonic and fetal brain, as well as glioma cells, were examined with respect to their susceptibility to HIV. CD4 antigen expression could be demonstrated only on glioma cells of the permanent glioma line 85HG-59 comprised of cells with properties characteristic of astrocytes. Nevertheless, normal embryonic and fetal brain cells as well as glioma cells could be infected by HIV as documented by immunocytochemical methods and southern blot analysis. HIV infected brain cells showed reduced growth rate and altered growth pattern. This study emphasizes the diversity of HIV conditioned CNS impairments, suggesting that genomic variability of HIV may result in varying cell type preference of the virus. The experimental data indicate that CD4 expression in brain cells is probably not 'conditio sine qua non' for HIV susceptibility. The alterations of HIV-infected brain cells demonstrated provide further evidence for a direct involvement of HIV in the pathogenesis of AIDS-related neurological syndromes.
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PMID:Evaluation of intracerebral lesions in patients with acquired immunodeficiency syndrome. Neuropathological findings and experimental data. 274 42

Over 35 intraaxial lesions in 15 patients suspected of having intracranial tumors were studied with MR before and after injection of Gadolinium-DTPA (Gd-DTPA). Diseases included primary and metastatic brain tumors, plaques of multiple sclerosis, occult arteriovenous malformations, lymphoma, toxoplasmosis, and pituitary adenoma. The precontrast T2-weighted sequence (SE 2000/30, 60) was found to be most sensitive in detecting intraaxial lesions, showing 17 lesions that were not seen on the post-Gd-DTPA T1-weighted sequence (SE 500/30). In one case of multiple sclerosis, several lesions seen on the pre-Gd-DTPA study on T2-weighted images faded after injection of Gd-DTPA (due to T2 shortening). In two patients with large metastatic foci, other small metastatic lesions were seen better after Gd-DTPA on both T1- and T2-weighted sequences. Four other patients with only one focal-enhancing lesion and one patient with multifocal lesions on T1-weighted images actually had a much larger single glioma depicted on pre-Gd-DTPA T2-weighted images. In a patient with AIDS, a ring-enhancing lesion thought to be an abscess proved to be lymphoma. The cryptic arteriovenous malformations enhanced but showed more characteristic findings, such as hemorrhage, on pre-Gd-DTPA studies. Our experience suggests that Gd-DTPA may not improve sensitivity of MR in the detection of intraaxial lesions. However, functional aspects of brain disease, such as the presence of perfusion of a lesion and active breach of the blood-brain barrier, are depicted well with Gd-DTPA and are vital for proper diagnosis in many instances.
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PMID:Gd-DTPA in clinical MR of the brain: 1. Intraaxial lesions. 349 Jul 58


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