Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0017636 (glioblastoma)
18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Empirical evidence in the clinical literature suggests that ionizing radiation influences human epileptic behavior. A group of patients with tumor-associated epilepsy, biopsy-proven malignancy, and primary antineoplastic treatment with ionizing radiation was selected to evaluate this observation. The antiepileptic effect of ionizing radiation was examined in 9 patients presenting with malignant cerebral tumor and medically refractory partial seizures during at least 2 months. Tissue diagnosis was obtained by stereotactic biopsy without further surgery. Histological categories included anaplastic astrocytoma (5 cases), glioblastoma (2), lymphoma (1), and metastatic non-small cell carcinoma of the lung (1). All patients had medically refractory simple partial seizures with or without secondary generalization with frequencies of 3/week to 8/day for 2-7 months before completion of therapy. Fractionated radiation therapy by parallel opposed fields was delivered with a cumulative dose range of 3,000-6,600 cGy. One patient also had 125I brachytherapy with implant removal after 6 months. Five patients had a seizure-free outcome for periods lasting 2-12 months, whereas the remainder experienced a reduction in frequency of greater than 75% during a follow-up period of 3 months to 6 years. One patient with a glioblastoma remained seizure-free for 3 months and experienced 2 generalized seizures during tumor progression and clinical deterioration but otherwise remained under good anticonvulsant control until his death after 1 year. This review of cases of partial seizures attributable to an unresected malignant cerebral tumor indicates that ionizing radiation may have a favorable effect upon medically refractory partial seizures with significant reduction or elimination of seizures. Moreover, the effect lasts beyond the immediate and early postradiation period. The therapy may thus also lessen the propensity for cerebral tissue towards later epileptogenicity that gives rise to a partial seizure disorder.
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PMID:Effect of ionizing radiation on partial seizures attributable to malignant cerebral tumors. 931 Oct 74

One hundred and nineteen consecutive patients affected by supratentorial gliomas were studied in order to determine the incidence of seizure at diagnosis, the occurrence of subsequent seizures and the efficacy of anticonvulsant treatment. The overall incidence of seizures as presentation symptom was 52% (62 patients). Preoperative seizures were present in 83% of patients affected by low-grade astrocytoma, in 46% of patients affected by anaplastic astrocytoma and in 36% of patients affected by glioblastoma. Postoperative epilepsy refractory to anticonvulsant treatment significantly related to low-grade histology and presence of preoperative seizures occurred in 48% of patients. Adverse effects associated with anticonvulsants were observed in 33.8% of patients treated with phenobarbital, 14.3% in the group treated with carbamazepine and 12% of patients treated with vigabatrin. We conclude that anticonvulsant treatment in patients affected by gliomas is often ineffective and prophylactic treatment should be discontinued after 6 months in patients preoperative seizures free. In patients with high risk of seizures antiepileptic drugs with good efficacy and lower incidence of adverse effects than phenobarbital are indicated.
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PMID:Epilepsy and gliomas: incidence and treatment in 119 patients. 1008 71

Elevated levels of extracellular glutamate ([Glu](o)) can induce seizures and cause excitotoxic neuronal cell death. This is normally prevented by astrocytic glutamate uptake. Neoplastic transformation of human astrocytes causes malignant gliomas, which are often associated with seizures and neuronal necrosis. Here, we show that Na(+)-dependent glutamate uptake in glioma cell lines derived from human tumors (STTG-1, D-54MG, D-65MG, U-373MG, U-251MG, U-138MG, and CH-235MG) is up to 100-fold lower than in astrocytes. Immunohistochemistry and subcellular fractionation show very low expression levels of the astrocytic glutamate transporter GLT-1 but normal expression levels of another glial glutamate transporter, GLAST. However, in glioma cells, essentially all GLAST protein was found in cell nuclei rather than the plasma membrane. Similarly, brain tissues from glioblastoma patients also display reduction of GLT-1 and mislocalization of GLAST. In glioma cell lines, over 50% of glutamate transport was Na(+)-independent and mediated by a cystine-glutamate exchanger (system x(c)(-)). Extracellular L-cystine dose-dependently induced glutamate release from glioma cells. Glutamate release was enhanced by extracellular glutamine and inhibited by (S)-4-carboxyphenylglycine, which blocked cystine-glutamate exchange. These data suggest that the unusual release of glutamate from glioma cells is caused by reduction-mislocalization of Na(+)-dependent glutamate transporters in conjunction with upregulation of cystine-glutamate exchange. The resulting glutamate release from glioma cells may contribute to tumor-associated necrosis and possibly to seizures in peritumoral brain tissue.
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PMID:Compromised glutamate transport in human glioma cells: reduction-mislocalization of sodium-dependent glutamate transporters and enhanced activity of cystine-glutamate exchange. 1059 60

A 74-year-old female with cerebral infarction and a 78-year-old female with cerebral glioblastoma suffered complex partial seizure. Ictal perfusion single photon emission computed tomography in these patients showed the interesting phenomenon of 'crossed cerebellar hyperperfusion,' a reversed crossed cerebellar diaschisis. The mechanism is probably spread of electrical seizure through efferent projections, and may be related to the cerebellar atrophy seen in patients with long-standing partial epilepsy.
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PMID:Crossed cerebellar hyperperfusion in symptomatic epilepsy--two case reports. 1072 Dec 58

This report investigates the pharmacokinetics of cytosine arabinoside (Ara-C), methotrexate (MTX), nimustine (ACNU) and valproic acid (VPA) in cerebrospinal fluid (CSF) during CSF perfusion chemotherapy. A 28-year-old Japanese woman with disseminated glioblastoma was, on admission, on a stable oral regimen of prolonged-release VPA tablets (Depakene-R), 400 mg twice a day, for seizure control. Twelve courses of CSF perfusion chemotherapy with Ara-C, MTX, and ACNU were administered. Plasma samples and CSF samples via Ommaya reservoirs were obtained during the eleventh course of treatment. The Ara-C and ACNU concentrations were measured by HPLC. The MTX and VPA concentrations were measured by fluorescence polarization immunoassay. During CSF perfusion chemotherapy, the highest CSF concentrations of Ara-C, MTX, and ACNU were observed at the end of the perfusion and decreased in a monoexponential pattern. The half-lives of Ara-C, MTX, and ACNU were 2.65, 3.52, and 0.71 h, respectively. No anticancer drugs were detectable in plasma during CSF perfusion chemotherapy. Before CSF perfusion chemotherapy, the free VPA concentration in plasma was 14.4% of the total VPA concentration. The mean total and free VPA concentrations in plasma were 78.0+/-0.8 and 10.9-0.3 microg/ml, respectively. The free VPA concentrations in plasma and in CSF were of similar values. At the end of perfusion, the lowest free VPA concentration in CSF was 30.3% of that at the initiation of perfusion. The free VPA concentrations in CSF at 3, 7, 23, and 47 h after the end of perfusion were 79.8, 94.5, 100.9, and 100.9% respectively of that at the initiation of perfusion. During CSF perfusion chemotherapy, the ratio of free VPA concentrations to the total VPA in CSF was 86.3+/-6.9%. The VPA concentrations in CSF rapidly decreased during the CSF perfusion but recovered to pre-treatment levels within 7 h.
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PMID:Pharmacokinetics of cytosine arabinoside, methotrexate, nimustine and valproic acid in cerebrospinal fluid during cerebrospinal fluid perfusion chemotherapy. 1086 38

Somatic inactivation of PTEN occurs in different human tumors including glioblastoma, endometrial carcinoma and prostate carcinoma. Germline mutations in PTEN result in a range of phenotypic abnormalities that occur with variable penetrance, including neurological features such as macrocephaly, seizures, ataxia and Lhermitte-Duclos disease (also described as dysplastic gangliocytoma of the cerebellum). Homozygous deletion of Pten causes embryonic lethality in mice. To investigate function in the brain, we used Cre-loxP technology to selectively inactivate Pten in specific mouse neuronal populations. Loss of Pten resulted in progressive macrocephaly and seizures. Neurons lacking Pten expressed high levels of phosphorylated Akt and showed a progressive increase in soma size without evidence of abnormal proliferation. Cerebellar abnormalities closely resembled the histopathology of human Lhermitte-Duclos disease. These results indicate that Pten regulates neuronal size in vivo in a cell-autonomous manner and provide new insights into the etiology of Lhermitte-Duclos disease.
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PMID:Pten regulates neuronal soma size: a mouse model of Lhermitte-Duclos disease. 1172 27

In order to investigate the clinical characteristics, neuroimaging findings, pathological features, treatment, and outcomes, and to provide valuable guidance for the diagnosis and management of intracranial gangliogliomas, 34 cases of intracranial gangliogliomas were retrospectively analyzed. This study included 23 males and 11 females. Age at operation ranged from 17 days to 50 years. All patients had preoperative magnetic resonance imaging (MRI). Computed tomography (CT), magnetic resonance spectroscopy (MRS), 18F-FDG-PET (positron emission tomography), and 99Tc-HMPAO-SPECT (single photon emission computed tomography) were also performed in some cases. All pathological specimens and all available neuroimages were re-evaluated. The follow-up period varied from 12 to 89 months (mean 36 months). Seizure was the most common presenting symptom (85%). Tumor calcification was detected by CT scan in six of 11 cases. Seventeen gangliogliomas (50%) showed cystic components and 18 tumors (53%) were enhanced on MRI. All temporal lobe gangliogliomas were located intracortically and most of them had poor demarcation on MRI. In comparison with the contralateral normal area, the gangliogliomas showed a reduced Cho/Cr and NAA/Cr ratio, and an increased Cho/NAA ratio. On 18F-FDG-PET, gangliogliomas were usually hypometabolic. HMPAO-SPECT indicated tumor hypoperfusion or isoperfusion. A gross total resection was achieved in 25 patients. Tumor progression was observed in three patients who underwent an incomplete tumor resection. Two of them underwent a malignant transformation to a glioblastoma. Twenty-seven patients could carry on their normal life activity with the Karnofsky Performance Scale (KPS) of more than 80. Even though ganglioglioma is a slowly growing benign tumor, which could be demonstrated by magnetic resonance spectroscopy (MRS), PET, and SPECT, there is a chance of malignant transformation, especially in cases of incomplete tumor resection. Gangliogliomas should be resected gross totally, if feasible, to achieve the best long-term outcomes.
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PMID:Intracranial ganglioglioma: preoperative characteristics and oncologic outcome after surgery. 1224 Nov 12

Epileptic seizures are common in patients with cerebral metastases as well as in patients with primary brain tumors. In cancer patients without primary brain tumors or brain metastasis, epileptic seizures may occur due to metabolic or toxic causes, or due to infections. We performed a retrospective analysis from our neurooncological database concerning the occurrence of seizures in patients with primary brain tumors, patients with cerebral metastases and in cancer patients without brain tumors. Patients with low grade gliomas, such as astrocytoma WHO I + II (69%), oligodendroglioma WHO II (50%), and mixed glioma WHO II-III (56%) were more likely to have seizures than patients with anaplastic glioma WHO III (44%), glioblastoma WHO IV (48%) or meningeoma (45%). In patients with brain metastasis, melanoma (67%), cancer of the lung (29%), and gastrointestinal tumors (21%) were the primaries with the highest frequency of seizures. In cancer patients without brain metastases or primary brain tumors, seizures occurred in 4%. In conclusion, the occurrence of epileptic seizures in patients suffering from primary brain tumors, as well as in patients with cerebral metastases, varied within the tumor entity. Therefore, especially in brain tumors where a higher probability of epileptic seizures is expected, they should be taken into account in the care of cancer patients.
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PMID:[The frequency of seizures in patients with primary brain tumors or cerebral metastases. An evaluation from the Ludwig Boltzmann Institute of Neuro-Oncology and the Department of Neurology, Kaiser Franz Josef Hospital, Vienna]. 1252 23

Malignant gliomas arise from two distinct pathways, as de novo lesions or from secondary transformation from low-grade lesions. Herein, we describe the cases of two patients to illustrate the proposition that de novo malignant gliomas can originate as non-enhancing tumors and rapidly progress to a pattern of ring enhancement characteristic of a glioblastoma. Both patients presented with new-onset seizures (simple partial and generalized). Their neurological examinations were unremarkable. Initial MRI evaluations revealed a right precentral gyrus and right medial temporal lobe lesions in each case, respectively. These lesions demonstrated increased T2 signal changes without contrast enhancement. The biopsy of the right frontal lesion in the first patient was consistent with an anaplastic astrocytoma; the second patient was followed expectantly. Repeat MRI for both patients within 17 weeks disclosed ring-enhancing lesions, consistent with an unusually rapid evolution to glioblastoma multiforme (GBM). Subsequent resection of the right medial temporal lesion in the second patient revealed a GBM. Neither tumor displayed abnormal overexpression of P53 by immunohistochemistry. Early MRI of de novo glioblastomas may demonstrate a non-enhancing tumor suggestive of a low-grade lesion. These tumors can rapidly evolve into ring-enhancing lesions more consistent with the traditional imaging findings.
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PMID:Non-enhancing de novo glioblastoma: report of two cases. 1544 98

The objective was to set the basis for a prospective, multicentre data collection on newly diagnosed adult glioblastoma patients diagnosed in Lombardia by means of a common database used by neurological and neurosurgical units of various hospitals, providing epidemiological, therapy and follow-up data. All adult patients with a newly diagnosed glioblastoma in 9 Lombardia hospitals from 31 March 2003 to 31 March 2004 were followed prospectively by a form elaborated by the Lombardia Neuro-oncology Group. Demographic data were recorded, as well as symptoms at onset, entity of tumour resection, post-surgical Karnofsky Performance Score, radio- and chemotherapy, presence/absence of venous thrombosis, type of antiepileptic treatment, time to tumour progression and survival time (ST). One hundred and thirty-four newly diagnosed glioblastoma patients were enrolled during the first year of the study. Male/female ratio was 1.6:1. Median age was 61 years. The most common single sign/symptom at disease onset included seizures, followed by mood/cognition changes and headache. In 71 patients, the tumour involved 1 brain lobe at diagnosis. Twenty-five patients underwent biopsy, 51 partial removal and 51 grossly total removal. At analysis of predictive value on ST, grossly total resection and chemotherapy were significantly associated with a longer ST. Age younger than 50 showed a trend to predictive value. A very high proportion of patients were treated with antiepileptic drugs, even in the absence of seizures. Median ST was 12 months in our cohort. Data in newly diagnosed glioblastoma patients in Lombardia are in line with other case series reported in other populations.
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PMID:A multicentre prospective collection of newly diagnosed glioblastoma patients in Lombardia, Italy. 1619 49


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