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 abnormal auditory brainstem responses (ABR) of 56 cases who had different retrocochlear disorders were analysed. These disease included acoustic neuroma, glioma, cholesteatoma, astrocytoma, meningoma in cerebellopontile angle (CPA), chromaffin tumor of jugular foramen, intracranial metastatic tumor, demyelinating disease, multiple cranial nerve paralysis, hepatolenticular degeneration, other CPA tumors, expansion or stenosis of internal auditory meatus (IAM), and so on. The ABR features were varied in these diseases, even in same disease. In general, the wave latencies and interwave periods prolonged in the disorders which occupied place in CPA, the differentiation of wave was not clear and/or the wave was not well repeated in the disorders which spreaded all over the brain. The cause of abnormal ABRin which CT and/or MRI were normal was also analysed. The ABR detection is a sensitive indication in retrocochlear lesions.
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PMID:[The analysis of abnormal auditory brainstem responses]. 927 2

Defective copper excretion in Wilson's disease can result in increased neurological copper concentrations. This is thought to occur following exposure to increased circulating copper released from necrotic hepatocytes in a saturated liver. BU17 human glioma cells and SH-SY5Y human neuroblastoma cells were exposed to media supplemented with copper in the range 0-250 microM for periods up to 48 h to investigate this hypothesis. Copper uptake, cell growth, intracellular radical generation, and oxidative stress were measured in copper exposed cells. No increase in copper uptake or inhibition of cell growth could be measured in either cell type at any time point or copper concentration investigated. However, significant increases in radical generation (p < 0.001) could be measured in both BU17 and SH-SY5Y cells. A decreased ability to cope when the cells were exposed to additional pro-oxidants suggested that the cells were under oxidative stress with significant reductions in cell viability following exposure to both copper and ascorbic acid. These data suggest that copper sequestration does not occur in neuronal cells exposed to elevated extracellular copper concentrations.
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PMID:The response of neurones and glial cells to elevated copper. 1147 Mar 18

Penicillamine is an oral agent used to treat intracerebral copper overload in Wilson's disease. Copper is a known regulator of angiogenesis; copper reduction inhibits experimental glioma growth and invasiveness. This study examined the feasibility, safety, and efficacy of creating a copper deficiency in human glioblastoma multiforme. Forty eligible patients with newly diagnosed glioblastoma multiforme began radiation therapy (6000 cGy in 30 fractions) in conjunction with a low-copper diet and escalating doses of penicillamine. Serum copper was measured at baseline and monthly. The primary end point of this study was overall survival compared to historical controls within the NABTT CNS Consortium database. The 25 males and 15 females who were enrolled had a median age of 54 years and a median Karnofsky performance status of 90. Surgical resection was performed in 83% of these patients. Normal serum copper levels at baseline (median, 130 microg/dl; range, 50-227 microg/dl) fell to the target range of <50 microg/dl (median, 42 microg/dl; range, 12-118 microg/dl) after two months. Penicillamine-induced hypocupremia was well tolerated for months. Drug-related myelosuppression, elevated liver function tests, and skin rash rapidly reversed with copper repletion. Median survival was 11.3 months, and progression-free survival was 7.1 months. Achievement of hypocupremia did not significantly increase survival. Although serum copper was effectively reduced by diet and penicillamine, this antiangiogenesis strategy did not improve survival in patients with glioblastoma multiforme.
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PMID:Phase 2 trial of copper depletion and penicillamine as antiangiogenesis therapy of glioblastoma. 1605 99