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)

A case of progressive multifocal leukoencephalopathy (PML) is reported, detected at autopsy of a 30-year-old patient. The clinical picture was characterized by a progressive course of mental deterioration and ingravescent neurological symptoms. The patient was HIV-negative. He died of bronchopneumonia, after a clinical course of 13 months. Autopsy disclosed pulmonary tuberculosis with involvement of regional lymph nodes. In the brain, besides numerous PML-foci of varying age and structure, a pleomorphic astrocytoma was found in the white matter of the right parietal lobe. In the brain stem glial proliferation resembling diffuse gliomatosis was also present. In situ hybridization revealed Papova-virus (JCV) in oligoglial nuclei, but not in neoplastic astrocytes. This is the third report on the concomitant occurrence of PML and glioma in man.
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PMID:Progressive multifocal leukoencephalopathy and gliomas in a HIV-negative patient. 130 Jun 8

We have initiated a study to identify host proteins which interact with the regulatory region of the human polyomavirus JC (JCV), which is associated with the demyelinating disease, progressive multifocal leukoencephalopathy. We examined the interaction of nuclear proteins prepared from different cell lines with the JCV regulatory region by DNA binding gel retardation assays. Binding was detected with nuclear extracts prepared from human fetal glial cells, glioma cells, and HeLa cells. Little or no binding was detected with nuclear extracts prepared from human embryonic kidney cells. Competitive binding assays suggest that the nuclear factor(s) which interacted with the JCV regulatory region was different from those which interacted with the regulatory region of the closely related polyomavirus SV40. We found three areas in the JCV regulatory region protected from DNase I digestion: site A, located just upstream from the TATA sequence in the first 98-base pair (bp) repeat; site B, located upstream from the TATA sequence in the second 98-bp repeat; and site C, located just following the second 98-bp repeat. There were some differences in the ability of the nuclear factor(s) from the two brain cell lines and HeLa cells to completely protect the nucleotides within the footprint region. The results from the DNase I protective studies and competitive DNA binding studies with specific oligonucleotides, suggest that nuclear factor-1 or a nuclear factor-1-like factor is interacting with all three sites in the JCV regulatory region. In addition, the results suggest that the nuclear factor which interacts with the JCV regulatory region from human brain cell lines is different from the factor found in HeLa cells.
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PMID:Interaction of a nuclear factor-1-like protein with the regulatory region of the human polyomavirus JC virus. 254 Jan 70

Immunofluorescent stains for fibronectin (FN) and glial fibrillary acidic protein (GFAP) were used in conjunction with routine histologic stains to study tumors induced in squirrel and owl monkeys by JC virus from progressive multifocal leukoencephalopathy (PML). Three varieties of glioma were identified. The first and most common variety was a neoplasm similar to grade 4 astrocytoma in humans. The second had thin, normal-appearing FN-positive vessel walls and a vastly expanded neuroectodermal parenchyma which could not be characterized by routine histologic stains. Anti-GFAP revealed the glial nature of the parenchyma. Isolating glial parenchymal cells from divergent FN-positive cells has become important to neurooncology. This type of tumor may be of particular interest for such isolations due to its high ratio of glial cells to divergent cells. The third variety was not a homogeneous neoplasm. It occurred as focal regions within tumors of the first type, and consisted of giant cells with huge nuclei. These cells resemble the cells of a human giant cell glioblastoma and bear a slight similarity to the bizarre glial cells seen in PML. The rare human giant cell glioblastoma might have an association with JC virus or with PML.
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PMID:Glial and divergent cells in primate central nervous system tumors induced by JC virus isolated from human progressive multifocal leukoencephalopathy (PML). 630 61

A brief outline is given of applications of immunohistological techniques to the study of normal and diseased nervous tissue. Protease treatment of paraffin sections usually enhances sensitivity and reliability both of IF and PAP techniques. Sensitivity of immunohistological examination of paraffin sections is comparable to that of virus detection by normal virological techniques in animal rabies and slightly superior to EM search for virions in SSPE and PML. Immunostaining for MBP appears to be the most sensitive method for myelin, especially for demonstration of very thin myelin sheaths, which are important in studies of myelogenesis and cortical myeloarchitecture. Prolonged fixation in formalin clearly diminishes or abolishes immunoreactivity. Compacted myelin stains less well for MBP than preparative myelin artefacts and the surface of myelinated fibers. GFAP production is enhanced when glioma cells invade surrounding mesenchymal structures. The chance finding of GFAP-like immunoreactivity in a cancer metastasis casts doubt on the astroglial specificity of GFAP.
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PMID:Immunohistological demonstration of serum proteins and structural and viral antigens in paraffin sections of nervous tissues. 637 89

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

JC virus causes the human demyelinating disease progressive multifocal leukoencephalopathy by selective infection of glial cells. This cell specificity results from glial-specific expression of viral early genes (large and small T antigens). Analysis of transcriptional regulation by the MH1 JC virus early promoter demonstrates that glial specificity is directed by the basal promoter. Because T antigen regulates the basal region of several viral and cellular promoters, we investigated whether it controls the JC virus basal promoter in a glial-specific manner. A JC virus T antigen expression plasmid generated a 95-kDa protein which exhibited nuclear localization and physical association with p53. T antigen repressed the JC virus and SV40 early promoters 4- to 5-fold in glioma cells. Conversely, T antigen induced 100- to 200-fold activation of the JC virus early promoter in nonglial cells, whereas the SV40 promoter was repressed. Activation required the JC virus TATA box sequence and a pentanucleotide repeat immediately upstream of the TATA box, but was independent of the upstream enhancer region. These data demonstrate that the JC virus basal promoter is responsible for glial-specific gene expression and suggest a mechanism for this regulation.
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PMID:Cell-specific activation of the glial-specific JC virus early promoter by large T antigen. 776 22

The etiologic agent of progressive multifocal leukoencephalopathy, a subacute demyelinating disease of the central nervous system, is the human polyomavirus JC virus (JCV), which causes a lytic infection of myelin-producing oligodendrocytes. In infected individuals the JCV genome can be detected in brain tissue and B lymphocytes isolated from the blood, bone marrow, or lymph nodes. Using mobility shift assays and a radiolabeled oligonucleotide from the JCV promoter-enhancer region (JCV bp 130 to 160), referred to as domain B, we were able to detect specific bands of the same mobility in nuclear extracts from human fetal glial cells, U-251 glioma cells, different B-cell lines, and in vitro-activated tonsillar B lymphocytes but not from T cells. In addition, a specific shift was detected when using nuclear extracts from freshly isolated tonsillar or lymph node B cells from five AIDS patients, two of whom later developed progressive multifocal leukoencephalopathy. Somewhat surprisingly, the above gel shift was partially inhibited by unlabeled oligonucleotides containing a kappa E2-binding site. UV cross-linking of the protein-DNA complex from either B cells or glial cells and analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed the presence of a 46-kDa band. Transient transfection of a reporter plasmid constructed by fusing a trimer of the domain B sequence to a minimal promoter revealed activity in B lymphocytes and glial cells but not in T cells. Mutational analysis of this region demonstrated that the core TGGC repeat was essential for enhancer activity. Thus, a similar protein in B lymphocytes and glial cells may account for the preferential replication of JCV in these two cell types.
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PMID:Regulation of JC virus expression in B lymphocytes. 825 31

Progressive multifocal leukoencephalopathy is a subacute demyelinating disease of the central nervous system due to an opportunistic infection by a polyomavirus, most often JC virus, which predominantly infects oligodendrocytes. Progressive multifocal leukoencephalopathy used to be a rare condition, usually complicating lymphoproliferative diseases. Since the onset of the AIDS epidemic, its incidence has considerably increased and HIV infection has become, by far, the main risk factor for the disease. In AIDS patients, progressive leukoencephalopathy frequently shows atypical clinical and pathological features. The development of malignant glial tumors, within demyelinating regions, in patients with progressive multifocal leukoencephalopathy, has been reported in exceptional cases. The course of progressive multifocal leukoencephalopathy is invariably fatal. The diagnosis can only be made with certainty by histopathological examination of the brain, on cerebral biopsy or at postmortem. However, neuroradiological features may be extremely suggestive in many cases and PCR seems to be a reliable technique for demonstrating viral genome in the CSF. A few antiviral treatments have been proposed, however their efficacy is difficult to assess due to the low prevalence of the disease and the occurrence of rare cases with spontaneously prolonged survival.
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PMID:[Progressive multifocal leukoencephalopathy: virological and neuropathological aspects]. 938 4

Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disease that results from an oligodendrocyte infection caused by JC virus. The JC virus early promoter directs cell-specific expression of the viral replication factor large T antigen, and thus transcriptional regulation constitutes a major mechanism of glial tropism in PML. We have previously demonstrated that T antigen controls the JC virus basal promoter in a glial cell-specific manner, since T antigen repressed the JC virus and simian virus 40 (SV40) early promoters in glioma cells but induced strong activation of the JC virus early promoter in nonglial cells. To further analyze these findings, T antigen and nuclear extracts from glial and nonglial cells were used to examine DNase I footprints on the proximal promoter. T-antigen binding to site II was more extensive than expected based on sequence homology with SV40, and nuclear proteins protected several regions of the proximal promoter in a cell-specific manner. Multiple Sp1 binding domains were identified. Site-directed mutagenesis revealed that T-antigen-mediated activation required a TATA box sequence, a pentanucleotide repeat immediately upstream of the TATA box, and an Sp1 binding site downstream of the TATA box. When footprints were obtained with mutant promoters which blocked T-antigen-induced transactivation, no change in T-antigen binding was observed. These results suggest that T antigen activates the JC virus basal promoter in nonglial cells by interaction with the transcription initiation complex.
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PMID:Glial cell-specific regulation of the JC virus early promoter by large T antigen. 1062 37

A 61-year-old man with no history of HIV infection developed a subacutely progressive dementia and left hemiparesis. Brain MRI showed a high intensity lesion in the right frontal lobe on T2 weighted image. There was no contrast enhancement after gadolinium-DTPA administration. 1H MRS revealed a marked decrease in the n-acetyl aspartate/creatine ratios and an increase in the choline/creatine ratio. A lactate peak also was present. A low-grade glioma was suspected and he was admitted to our hospital. On examination, there was a mild dementia and left hemiparesis. A peripheral blood count revealed lymphocytopenia (426/mm3) with a CD4/CD8 ratio of 0.28. No evidence of HIV infection, malignancies or collagen disease was found. A brain biopsy revealed no tumor cells but instead demyelinated brain tissue with large nucleated cells. JC virus antigen was detected in the cells of the demyelinated lesions. A diagnosis of PML associated with idiopathic CD4 positive lymphocytopenia was made. There are only a few reports concerning 1H-MRS findings in patients with PML and the present case illustrates the difficulty of making a differential diagnosis between PML and glioma.
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PMID:[Progressive multifocal leukoencephalopathy with idiopathic CD4 positive T-lymphocytepenia mimicking a low grade glioma on proton MR spectroscopy. A case report]. 1624 99


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