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)

An increase in the incidence of malignant gliomas has been noted over the last two decades. Chemotherapy, either adjuvant or at recurrence, has extended the survival of patients with malignant gliomas. Oligodendrogliomas and anaplastic astrocytomas represent the most chemosensitive tumors, while glioblastomas have been relatively resistant to any treatment modality. The most active agents include carmustine, procarbazine, and eflornithine, and combinations such as lomustine, procarbazine and vincristine, or thioguanine, dibromodulcitol, procarbazine, lomustine, fluorouracil and hydroxyurea. Although chemotherapy has demonstrated some efficacy against malignant glioma, new therapeutic strategies are needed for this devastating disease.
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PMID:Chemotherapy for malignant gliomas. 821 33

We identified 39 patients with chronic epilepsy (seizures > or = 2 years) proven to have primary brain tumors. These cases represent approximately 12% of the surgery cases for epilepsy in the same period. Mean age of seizure onset was 13.2 years: mean duration before operation was 10.5 years. Thirty-eight of 39 had normal neurologic examination. Twenty-six tumors were temporal, 7 were frontal, 4 were parietal, and 2 were occipital. Nine of 26 (34.6%) of the temporal group had contralateral interictal EEG spikes. Pathology was 15 ganglioglioma, 13 low-grade astroctoma, 4 oligodendroglioma, 2 low-grade mixed glioma, 1 pleomorphic xanthoastrocytoma, 2 dysembryoplastic neuroepithelial tumor, and 1 ependymoma. Postoperative seizure frequency (minimum follow-up 6 months) ranged from 15 to 16 seizure-free auras only in patients with temporal tumors and total gross tumor removal (mean follow-up 28 months) to 0 of 6 seizure-free in patients with extratemporal tumors who underwent subtotal resection or biopsy.
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PMID:Chronic intractable epilepsy as the only symptom of primary brain tumor. 824 54

We have previously shown that alpha B-crystallin is a heat-shock protein which specifically accumulates in response to the expression of c-Ha-ras and v-mos oncogenes in mouse NIH 3T3 fibroblasts. Elevated levels of alpha B-crystallin mRNA or protein were shown to be associated with pathological conditions of the brain. Therefore, we have examined the expression of alpha B-crystallin in normal human brains and brain tumors by Western blot analysis. alpha B-crystallin is moderately expressed in adult but not fetal brain. Elevated levels of alpha B-crystallin expression are observed in glial tumors such as astrocytoma, glioblastoma multiforme, and oligodendroglioma. alpha B-crystallin in these tumors is predominately unphosphorylated. High amounts of accumulated alpha B-crystallin in astrocytic tumors are preferentially found in the more aggressive stages. Glioblastoma multiforme is exceptional in that high alpha B-crystallin expression is observed in only one half of the analyzed samples whereas no alpha B-crystallin could be detected in the other. These results indicate that alpha B-crystallin may be a useful biochemical marker for studying the pathogenesis of various human brain tumors.
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PMID:Expression of alpha B-crystallin in human brain tumors. 824 72

From 1973 to 1990, 67 patients with a diagnosis of low-grade glioma were treated in our hospital. Overall survival was analysed as well as the influence of patient, tumour- and treatment-related factors with special focus on tumour volume parameters. Our study group included 49 patients treated by surgery and post-operative radiotherapy (RT) (40 patients) or post-biopsy irradiation alone (9 patients). Total or almost total resection was performed in 16 patients; partial excision was done in 24. With the available pre-surgery and pre-RT CT-scan and/or MRI images we were able to calculate tumour volumes by measuring the largest tumour dimensions in the three axes D1, D2, D3 and by assuming an ellipsoidal growth (i.e., tumour volume = D1D2D3 pi/6). RT was delivered to involved regions: either the residual tumour volume or the tumour bed. The median RT dose was 56 Gy (45-60, range). The 60- and 90-month overall survival (Kaplan-Meier) was 79% and 67%, respectively. Female sex, > 70% Karnofsky (Kf) score, oligodendroglioma and < 71 cm3 (approximately 5 cm diameter sphere) tumour residuals before RT were associated with better overall survival rates (p < 0.05, log-rank). However, a Cox proportional hazards model showed that only the histological subtype and Kf significantly determined the patients' outcome: 60-month overall survival of 100%, 62%, 83% and 64% for oligodendrogliomas, mixed oligo-astrocytomas and grade-I and grade-II astrocytomas, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Radiotherapy for supratentorial low-grade gliomas: results and prognostic factors with special focus on tumour volume parameters. 835 20

The extraneural spreading of gliomas is an infrequent occurrence which is not necessarily related to either tumor histology or site. This paper reports two cases, a glioblastoma and an oligodendroglioma, both presenting extradural diffusion. In the first case, where there was severe intracranial hypertension, the tumor found its way out from the neurocranium, far from the site of the operation, perforating the dura and the bone of the cranial base. In the second case, the operation may have facilitated the extraneural invasion. This unusual behaviour of glial tumors is probably less rare than presumed. It may go unnoticed if the attention is concentrated on the usually severe neurological syndrome which is present in these patients.
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PMID:The transdural extension of gliomas. 845 64

To examine the potential of AAV as a vector for gene transfer in glial cells, an established astrocytoma cell line and short-term cultures derived from human oligodendroglioma have been coinfected with AAV and helper adenovirus. The level of AAV replication in glioma cells was high indicating that they express receptors for AAV.
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PMID:Adeno-associated virus (AAV) as a vector for gene transfer into glial cells of the human central nervous system. 854 26

We describe the clinical and neuroradiological findings in a 63-year-old man with Parinaud's syndrome. Magnetic resonance (MR) imaging showed a mass lesion within the quadrigeminal plate. Additional MR findings included a right frontoparietal subcortical lesion as well as periventricular white matter edema due to acute deterioration of hydrocephalus. On MR, the diagnosis of multifocal glioma was proposed. Neuropathological examination after resection of the supratentorial lesion revealed an oligodendroglioma, grade II.
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PMID:Parinaud's syndrome in a patient with multifocal glioma. 864 84

We present the results of a retrospective survey of 1,218 patients treated at the Norwegian Radium Hospital during the years 1980-94 for primary tumours of the central nervous system. Median survival for patients with glioblastoma (n = 492) was 12 months, for patients with anaplastic astrocytoma (n = 83) 25 months, astrocytoma (n = 260) 95 months, oligodendroglioma (n = 85) 74 months, mixed glioma (n = 68) 65 months, and medulloblastoma (n = 53) 109 months. Median survival for patients with brain stem tumours (n = 37) was nine months, while 74% of patients with tumours in the pineal region (n = 38) survived for five years. The histology and localisation of the tumour, as well as age and functional status, are important prognostic factors for survival in patients with primary CNS tumours.
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PMID:[Prognosis in primary tumors of the central nervous system. A patient material from the Norwegian Radium Hospital 1960-94]. 865 12

In 1991-1993, 52 patients underwent surgery for low-grade supratentorial glioma. In 37 of them (astrocytoma 22, oligodentrocytoma 12, oligodendroglioma 2) seizures, often refractory to drug therapy, appeared as the first symptom. These cases were retrospectively analyzed. The patients had partial seizures: simple, complex, or secondarily generalized (preoperative duration: from 3 days to 17 years (mean 2 years); frequency: between 1 and 2/year and over 10/day). Neurological examination either revealed slight focal changes or was normal. Conventional craniotomy and resection of a tumor, without intraoperative electrocorticography, was performed. Partial resection was performed in 73%, subtotal in 5%, "total" in 22% of the cases. Postoperatively, 27 patients had focal radiotherapy, 3 of them in combination with chemotherapy. Two patients were reoperated. Out of 33 alive (89%), about two-thirds appear normal by neurological examination and are seizure-free at present (mean follow-up period 28 months). Most remain on antiepileptic drugs at lower doses. Histological and immunohistochemical analyses of resected tissue together suggest that the peripheral zone of cortical tumor infiltration may participate on epileptogenesis.
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PMID:Epilepsy associated with low-grade brain glial neoplasms. 869 83

Because the percentage of dividing cells in malignant gliomas is small, cell cycle specific drugs such as VP16 are most effective if given continuously over prolonged periods. In this study, we chose a dose of 50 mg/day to minimize therapy interruptions for myelosuppression. VP16 was given until the neutrophil count dropped to < 1.0 x 10(9)/L or the platelets fell to < 75 x 10(9)/L and resumed when the counts rose to normal levels. We treated 46 patients with supratentorial malignant glioma (15 anaplastic astrocytoma, 21 glioblastoma multiforme, 9 anaplastic oligodendroglioma, 1 undifferentiated primary malignant brain tumor) at the time of tumor progression. All had KPS > or = 70 at study entry. All patients had prior RT, 13 with adjuvant nitrosourea. Twenty-four had prior nitrosourea chemotherapy for tumor progression, 7 had no prior chemotherapy. We treated 20 patients with VP16 at first progression and 26 at second or later progression. All patients had CT or MR scans and clinical evaluation every 8 weeks. Median time to tumor progression (TTP) was 8.8 weeks for all evaluable patients, 8.6 weeks for those treated at first progression and 8.4 weeks for those treated at second progression, 9.1 weeks for anaplastic astrocytoma, 7.5 weeks for glioblastoma multiforme and 17.1 weeks for anaplastic oligodendroglioma. There were 8 responses and 11 patients with stable disease for at least 8 weeks (R + SD = 42%). Prolonged low-dose oral VP15 is well tolerated, with minimal myelosuppression. Prolonged low-dose oral VP16 is modestly effective treatment for patients with recurrent malignant glioma and is more effective for anaplastic astrocytoma and anaplastic oligodendroglioma than glioblastoma multiforme.
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PMID:Phase II study of prolonged oral therapy with etoposide (VP16) for patients with recurrent malignant glioma. 869 37


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