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 clinical and pathological findiing in an adult with lead encephalopathy due to moonshine consumption are presented. The remarkable focality of of the edema led both the clinicians and radiologists to consider this a cerebral glioma.
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PMID:Lead encephalopathy simulating a cerebral neoplasm in an adult. Case report. 85 18

Phase III Trial 8,301 tested the efficacy and safety of intraarterial (IA) BCNU for the treatment of newly resected malignant glioma, comparing IA BCNU vs intravenous (IV) BCNU (200 mg/m2 q 8 wks), each regimen without or with IV 5-FU (1 g/m2/d x 3 two wks after BCNU). All patients also received radiation therapy. 505 patients entered the study; 448 were in the Valid Study Group (VSG). Excluding 190 patients who for medical reasons were not eligible for IA BCNU, 315 patients were randomized between IA (167) and IV (148) BCNU. Actuarial analysis (log-rank) demonstrated worse survival for the IA group (p = 0.002). Serious toxicity was observed in the IA group; 16 patients (9.5%) developed irreversible encephalopathy with CT evidence of cerebral edema, and 26 patients developed visual loss ipsilateral to the infused carotid artery. 5-FU did not influence survival. Survival between the IV and the IA BCNU patients with glioblastoma multiforme did not differ, but was worse for IA BCNU patients with anaplastic astrocytoma than for IV BCNU (p = 0.002). Neuropathologically, IA BCNU produced white matter necrosis. IA BCNU is neither safe nor effective. Phase II Trial 8420, compared IA cisplatin, 60 mg/m2 every 4 wks, vs IV PCNU, 100 mg/m2 q 8 wks; 311 patients were randomized. Preliminary results have been presented. Severe encephalopathy occurred in only 1.5% of patients receiving IA cisplatin. The median survival of the IV PCNU patients was 11.8 months; that of the IA cisplatin patients was 9.4 months, not statistically different.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chemotherapy of malignant gliomas: studies of the BTCG. 144 62

This Phase III trial tested the efficacy and safety of intra-arterial 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) for the treatment of newly resected malignant glioma, comparing intra-arterial BCNU and intravenous BCNU (200 mg/sq m every 8 weeks), each regimen without or with intravenous 5-fluorouracil (1 gm/sq m three times daily given 2 weeks after BCNU). All patients also received radiation therapy. A total of 505 patients were randomly assigned within the study. Fifty-seven patients were excluded, primarily because of neuropathology error, and the remaining 448 patients constituted the Valid Study Group. Of the total 505 patients, 190 patients could not receive intra-arterial BCNU and 315 patients were randomly assigned to receive intra-arterial (167 patients) and intravenous (148 patients) BCNU. Actuarial analysis (log-rank) demonstrated reduced survival for the intra-arterial group (p = 0.03). Serious toxicity was observed in the intra-arterial group; 16 patients (9.5%) developed irreversible encephalopathy with computerized tomography evidence of cerebral edema, and 26 patients (15.5%) developed visual loss ipsilateral to the infused carotid artery. Administration of 5-fluorouracil did not influence survival. The survival rate between the intravenous and the intra-arterial BCNU patients with glioblastoma multiforme did not differ, but was worse for intra-arterial BCNU patients with anaplastic astrocytoma than for those receiving intravenous BCNU (p = 0.002). Neuropathologically, intra-arterial BCNU produced white matter necrosis. It is concluded that intra-arterial BCNU is neither safe nor effective in prolonging survival when administered by the methods used in this study of newly diagnosed patients with malignant glioma.
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PMID:A randomized comparison of intra-arterial versus intravenous BCNU, with or without intravenous 5-fluorouracil, for newly diagnosed patients with malignant glioma. 156 40

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

We describe the neuropathologic findings at autopsy in six patients who developed a progressive encephalopathy complicating the treatment of malignant gliomas with combined intra-arterial 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and cerebral irradiation. Four brains were free of tumor and one contained a microscopic focus of residual glioma. In only one case was there evidence of tumor progression. A disseminated process characterized by miliary foci of necrosis with mineralizing axonopathy was present in all cases, restricted to the internal carotid distribution of the perfused hemisphere and involving primarily though not exclusively the white matter, which was diffusely and severely edematous. This was combined in 3 cases with a histologically dissimilar, massive necrotizing leukoencephalopathy indistinguishable from pure radionecrosis. Much of the toxicity of this therapy is mediated by vascular injury, but the disseminated necrotizing lesion probably reflects, at least in part, direct neural damage.
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PMID:Fatal necrotizing encephalopathy complicating treatment of malignant gliomas with intra-arterial BCNU and irradiation: a pathological study. 182 43

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

Increasingly vigorous chemotherapy of cancer including primary and metastatic central nervous system disease has resulted in prolonged good-quality survival. However, there has been an associated increase in neurotoxicity from both radiation therapy and chemotherapy. All classes of chemotherapeutic agents contain drugs that are potentially neurotoxic, often only at high doses. Mechlorethamine, the first nitrogen mustard, is not neurotoxic at conventional dosage, but at high doses, it may produce both an acute and a delayed encephalopathy. Methotrexate administered intrathecally often induces reversible aseptic meningitis, but chronic administration, either intrathecally or high-dose intravenously, may produce fatal leukoencephalopathy. 5-Fluorouracil at high dosage may cause cerebellar ataxia, but may also do so at low dosage when combined with thymidine infusions. Cytosine arabinoside at high dosage may also produce cerebellar ataxia. Vincristine produces a peripheral neuropathy, and less commonly causes both autonomic and cranial neuropathy. The enzyme L-asparaginase can produce a dose-related reversible encephalopathy. BCNU, now the mainstay of glioma chemotherapy, may combine with radiation to produce long-term cerebral atrophy. Both intracarotid and high-dose intravenous BCNU administration may cause encephalopathy. Several other chemotherapeutic agents have also been reported to cause neurotoxicity under certain circumstances.
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PMID:Neurological complications of antineoplastic therapy. 638 4

Iodine-123 labeled hydroxyiodopropyldiamine (HIPDm) is a diffusible indicator with an 85%-90% extraction fraction and stable retention in the brain for more than 2 hr. Equilibrium-phase imaging and quantitation using single-photon emission computed tomographic (SPECT) scanning defined a distribution of HIPDm in proportion to regional cerebral blood flow (rCBF). Studies in calves affirmed a close correspondence (r = 0.97) in calculated rCBF between HIPDm and microspheres using the tissue deposition-arterial input function microsphere methodology. Using this same mathematical analysis in vivo, reproducible rCBF data within the expected range of normal were obtained on repeated studies in the same nonhuman primate. With a diffuse encephalopathy secondary to subarachnoid blood, a bilaterally symmetric decrease in rCBF was present. A prominent focal decrease in HIPDm accumulation and calculated rCBF was noted with cerebral infarction in the distribution of a ligated middle cerebral artery. Patient studies with glioma revealed diminished HIPDm accumulation due to decreased flow and/or pH in the region of the neoplasm as well as in the associated vasogenic edema and overlying gray matter.
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PMID:In vivo quantitation of regional cerebral blood flow in glioma and cerebral infarction: validation of the HIPDm-SPECT method. 641 Aug

The present study was aimed at elucidating the effect of cyclosporine on phenylephrine-evoked nitric oxide (NO) production in C6 glioma cells using direct electrochemical NO monitoring. Phenylephrine (0.1-10 microM) dose-dependently stimulated NO production (0.8-12.9 microM) and this was blocked by NO synthase inhibitor, prazosin, Ca2+-depletion and Xestospongin C (a blocker of the inositol 1,4,5-trisphosphate (IP3) receptor), suggesting that the alpha1-adrenoceptor signaling pathway mediates NO production in C6 cells. Cyclosporine (approximately 10 microM) failed to evoke NO production but increased phenylephrine-evoked NO production by 20-120% of phenylephrine alone in a dose-dependent manner (1-5 microM). Xestospongin C, at a concentration which showed no effect on phenylephrine-induced NO production, significantly inhibited the cyclosporine-enhanced phenylephrine response. This finding suggests that cyclosporine may increase phenylephrine-induced NO production by accelerating IP3 receptor function in the alpha1-adrenoceptor signaling pathway in C6 cells. This enhanced NO production in glial cells may be operative for the occurrence of cyclosporine neurotoxicity including convulsions and encephalopathy.
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PMID:Cyclosporine enhances alpha1-adrenoceptor-mediated nitric oxide production in C6 glioma cells. 1106 17

To evaluate the influence of radiation volume and other risk factors for the development of delayed radiation toxicity in patients treated for low-grade glioma, a retrospective analysis of 41 adult patients treated with focal or whole brain radiotherapy (WBRT) was performed. For all patients CT and MRI scans were revised to quantify brain atrophy and white matter lesions. Medical data were reviewed concerning baseline and tumor characteristics, treatment, survival, signs and symptoms of clinical encephalopathy and cardiovascular risk factors. In patients treated with WBRT an increased risk was found for brain atrophy (RR 3.1), white matter lesions (RR 3.8) and clinical encephalopathy (RR 4.2). An increased risk of atrophy (RR 2.2) and white matter lesions (RR 2.9) was also found in patients aged over 40 years. Furthermore, brain atrophy and white matter lesions were more severe in patients treated with WBRT and in older patients. In conclusion, both the incidence and the severity of abnormalities is greater in patients treated with WBRT and in older patients.
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PMID:Delayed radiation toxicity after focal or whole brain radiotherapy for low-grade glioma. 1501 65


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