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 adult goat was examined because of behavioral changes and circling. Results of neurologic examination, CSF analysis, hematologic evaluation, and computed tomography of the brain were suggestive of an intra-axial mass. The goat was euthanatized because of worsening neurologic condition and poor prognosis. Necropsy revealed a large mass in the right cerebral hemisphere and caudal brain herniation through the foramen magnum. The mass was diagnosed as a glioma, with oligodendrocyte differentiation. Results of immunohistochemical evaluation were compatible with a malignant, poorly differentiated tumor.
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PMID:Glioma in a goat. 777 36

Ventriculolumbar perfusion of methyl 6-[3-(2-chloroethyl)-3-nitrosoureido]-6-deoxy-alpha-D-glucopyranoside (MCNU), a water soluble nitrosourea with log P -0.71, may be efficacious in the treatment of subarachnoid dissemination of malignant glioma. We used 2 dogs to study the neurotoxicity and pharmacokinetics of MCNU. MCNU (1 mg), dissolved in 10 ml of artificial CSF, was administered via the right lateral ventricle during a period of 18 to 42 min and the CSF was drained by lumbar puncture. The perfusion was repeated once a week for 10 consecutive weeks. No neurological and systemic symptoms were noted after perfusion. Histological examination of the brain and spinal cord showed local denudation of the ependyma and local subependymal spongy degeneration and gliosis in the lateral ventricle into which MCNU was administered in one dog and local denudation of the ependyma in the other. When administration was over a period of 21 to 38 min, the MCNU concentration in the lumbar CSF peaked at 11.11 to 50.67 micrograms/ml, in 28 to 78 min. The area under the drug concentration-time curve (AUC) was 1152 micrograms x min/ml on average, significantly larger than that of ACNU. The elimination phase followed linear kinetics and the half-time was 41.1 min on average, significantly longer than that of ACNU. These findings suggest that ventriculolumbar perfusion of MCNU may be effective in the treatment of subarachnoid dissemination of malignant glioma notwithstanding some local histological changes.
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PMID:Neurotoxicity and pharmacokinetics of ventriculolumbar perfusion of methyl 6-[3-(2-chloroethyl)-3-nitrosoureido]-6-deoxy-alpha-D-glucopyranoside (MCNU) in dogs. 780 74

Little information exists regarding which glioma cells are able to escape immune system detection and progress within the host. In order to elucidate some of the mediators which facilitate the growth and spread of glioma cells, the expression of cytokines, TNF-alpha, IL-6, gamma-IFN, IL-10, and GM-CSF, within 12 human glioma specimens was investigated by the polymerase chain reaction. The twelve patients with malignant glioma were categorized into a localized (n = 4) and an invasive glioma (n = 8) groups, mostly glioblastoma multiforme, based upon the CT and MRI scans. We examined the correlation between specific cytokine gene expression and the clinical category of each patient. The results showed that while IL-10 mRNA transcripts were expressed in most of the tumors from the invasive glioma group (7/8), they were not expressed in tumors from the localized group. On the other hand, gamma-IFN gene expression was more frequent in tumors from the localized group (3/4 vs 1/8 from the invasive group). The mRNA transcripts of IL-6 and GM-CSF were more frequently expressed in tumors from the localized group. No consistent pattern was seen in TNF-alpha gene expression between the two groups. Among the five cytokines studied, IL-10 mRNA was selectively expressed within invasive gliomas compared to less malignant, localized glioma group. Our results demonstrate specific cytokine mRNA profiles in glioma patients, which might have prognostic significance for immunotherapy.
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PMID:Selective expression of interleukin-10 gene within glioblastoma multiforme. 795 24

In 16 patients with 21 metastatic brain tumors and 9 patients with a malignant glioma, tumor volume, volume of the edematous tissue, edema production, speed of edema propagation and edema resolution were examined by using the CT. Edema production was determined according to a technique described previously and ranged between 0.09 and 1.63 ml/h in metastases and between 0.42 and 3.49 ml/h in gliomas. The speed of edema propagation ranged from 0.2-2.2 mm/h. Edema resolution can take place within the tissue (i.e. reabsorption into blood) as well by drainage into the ventricular or subarachnoid CSF. In a few small metastases with a small perifocal edema (without contact to the ventricule or the subarachnoid space) the amount of edema resolution within the tissue could be determined and averaged 0.0086 ml/h/cm3. This probably represents the reabsorption of edema fluid into capillaries within the edematous tissue. If this value is used to calculate the edema reabsorption in larger tumors, the resulting data are considerable lower than the respective edema production rate of that tumor. This indicates, that in larger tumors the main fraction of the edema fluid is draining into the ventricular and/or subarachnoid CSF.
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PMID:Formation and resolution of human peritumoral brain edema. 797 93

Nitrosoureas are the drugs most effective in the treatment of patients with intracerebral malignant glioma. Their limiting toxicity is delayed myelosuppression. A prospective, randomised crossover study of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) was performed in patients receiving BCNU for relapsed glioblastoma, to investigate whether the resulting haematological toxicity profile could be modified by rhGM-CSF. Adequate data for analysis were obtained in 13 patients. Following BCNU, the nadir neutrophil count was higher in 12 out of 13 patients during the rhGM-CSF-protected cycles compared with the unprotected cycles. The median nadir was also significantly higher (1.79, CI 0.76-3.52, P < 0.005). Five episodes of neutropenia (< 2 x 10(9) l-1) occurred during the unprotected cycles compared with none in the rhGM-CSF-protected cycles (P = 0.076). There was no evidence of any effect on platelets. This result shows that the haematological toxicity profile following therapeutic doses of BCNU can be modified. It suggests that rhGM-CSF and other growth factors should be investigated for clinical efficacy in chemotherapy using nitrosoureas.
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PMID:rhGM-CSF ameliorates neutropenia in patients with malignant glioma treated with BCNU. 812 85

More than 80% of malignant gliomas have been reported to recur locally after conventional chemoradiation therapy. This regional pattern of recurrence has encouraged the introduction of new treatments for local tumors. Since 1987 interstitial brachytherapy using Iridium-192 seeds has been carried out in our department for malignant brain tumors. The present study was designed to evaluate the patterns of recurrence following interstitial brachytherapy and to assess how this recurrence differs from that observed in patients treated by conventional means. Ten patients who satisfied the following criteria were selected among 41 patients treated with brachytherapy. The criteria were; 1) histologically diagnosed to be malignant glioma (astrocytoma grade III or glioblastoma), 2) followed up with MRI every month after the brachytherapy, 3) follow-up period was more than 6 months, and 4) the time of recurrence was confirmed. The patients were classified into 3 groups according to the patterns of tumor recurrence as follows; 1. Local recurrence group: The tumor recurred near the pretreatment tumor site. 2. Necrotomy group: Reoperation was performed because of neurological deterioration and radiographic evidence of increasing mass effect with surrounding edema. Neurological symptoms were unchanged or improving during the 6 months after the reoperation. 3. CSF seeding group: Primary tumor was well controlled, but seeding via cerebrospinal fluid was recognized on MRI. Local recurrence occurred in three patients, necrotomy was carried out in three patients, and CSF metastases were defined by both MRI and clinical symptoms in four patients. Median radiation does was 33 Gy in the local recurrence group, 57.6 Gy in the necrotomy group, and 43.2Gy in the CSF seeding group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Patterns of recurrence in malignant gliomas after brachytherapy]. 816 95

A five-and-a-half-year-old boy with neurofibromatosis had bilateral orbital optic gliomas visible on magnetic resonance imaging. Both tumors displayed a double-intensity signal characterized by a circumferential area of CSF-intensity tissue surrounding and sharply delimited from a central linear core of opposite signal intensity. The peripheral CSF-intensity signal in orbital optic glioma correlates with the histopathological finding of perineural arachnoidal gliomatosis and serves as a neuroradiologic marker for neurofibromatosis.
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PMID:The "pseudo-CSF" signal of orbital optic glioma on magnetic resonance imaging: a signature of neurofibromatosis. 823 1

CSF and plasma platinum levels were examined in patients with malignant glioma after administration of etoposide and cisplatin each at doses of 60 mg/m2 by 60-minute selective intraarterial infusion. These same factors were also examined in patients with metastatic brain tumors after administration of cisplatin at a dose of 60 or 100mg/m2 by 60-minute intracarotid or intravenous infusion. Plasma and CSF samples taken through an Ommaya reservoir placed in the lateral ventricle or postoperative cavity were analyzed for platinum content by atomic absorption spectroscopy. Plasma and CSF platinum levels were dose dependent. The overall plasma platinum curves were biphasic, with mean half-lives of 35 minutes and 56 hrs. The mean peak total CSF concentration was 10.0% of the peak total plasma platinum and 20.2% of the peak free plasma platinum in patients with malignant glioma. In patients with a solid metastatic brain tumor, the mean peak total CSF concentration was 1.9% of the peak total plasma platinum and 4.0% of the peak free plasma platinum after i.v. infusion. After intracarotid infusion, the mean peak total CSF concentration was 3.4% of the peak total plasma platinum and 7.0% for the peak free plasma platinum. In patients with meningeal carcinomatosis, the mean peak CSF concentrations were 7.7% of the peak total plasma platinum and 13.7% of the peak free plasma platinum. The free to total platinum ratio in plasma decreased quickly and that in CSF increased and was maintained at the high levels of 80% for two hours or more.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pharmacokinetics of plasma and cerebrospinal fluid cisplatin in patients with malignant glioma and metastatic brain tumor after selective intraarterial or intravenous and intracarotid administration of etoposide and cisplatin]. 829

The feline infusion model of brain edema was used to evaluate the pathophysiological effects of 0.6 ml infusions of autologous serum protein (66%), human serum protein (66%), human glioma cyst fluid and a tissue culture medium (TCM) on the structure and function of the forebrain white matter. These infusions increased local white matter water content by between 10.8 and 12.5 ml/100 g brain and were associated with moderate increases in ICP and CSF outflow resistance and a significant decrease in lumped craniospinal compliance. Cortical somatosensory potentials, motor evoked potentials, EEG and local cerebral blood flow (rCBF) at normocapnia were generally unchanged by the various infusions. All infusates except the 66% autologous serum protein infusion impaired rCBF CO2 reactivity. Histologically all infusates caused marked extracellular edema. The autologous serum protein infusion caused no additional histological changes whereas the glioma cyst infusates caused profound endothelial and astrocytic swelling, focal endothelial necrosis, basement membrane disruption, perivascular microglial reaction and pavementation and perivascular migration of polymorphonuclear leukocytes. Similar but less marked changes were seen after infusion of human serum protein whilst the TCM produced only minimal changes. The intensity and extent of Evans Blue extravasation into the forebrain white matter was greatest with glioma cyst infusates and with all infusions reflected the extent to microvascular changes. These studies show that products derived from gliomas cause additional damage to the blood-brain-barrier than that caused by non-autologous serum proteins. These results add further support for the existence of glioma derived permeability factors (GDPF), but suggest neither serum proteins nor glioma derived compounds in the white matter interstitium significantly influence local electrophysiological function. Some limitations of the infusion edema model when using non-autologous infusions and difficulties quantitating brain dysfunction are emphasised.
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PMID:Neuropathological and neurophysiological effects of interstitial white matter autologous and non-autologous protein containing solutions: further evidence for a glioma derived permeability factor. 846 May 70

The appropriate management of brainstem tumors in patients with neurofibromatosis 1 (NF1) has been problematic because the natural history of these lesions remains poorly defined. To formulate rational guidelines for the evaluation and treatment of these tumors, we reviewed the outcome of 21 patients with brainstem mass lesions followed in our NF clinic during the last 9 years. We subdivided the imaging features of these lesions into four groups: (1) diffuse enlargement of the brainstem with hypointensity on T1-weighted MR images and hyperintensity on T2-weighted images (n = 9); (2) focal enhancing masses (n = 7); (3) intrinsic tectal tumors (n = 5); and (4) focal nonenhancing areas of hypointensity on T1-weighted MR images (n = 2). Two cases exhibited two types of lesions. Twelve patients presented with, or developed, symptoms that were referable to the mass; in nine, the lesion was asymptomatic. A distinguishing feature of these tumors was their generally indolent biological behavior. With a median follow-up of 3.75 years, only 10 patients have had radiographic (n = 9) or clinical (n = 3) evidence of disease progression. In seven of these patients, the tumor subsequently stabilized in size or regressed without intervention. Only four patients, each with a focal enhancing tumor, received specific therapy for the tumor; this consisted of biopsy (n = 1), excision (n = 3), and adjuvant radiotherapy (n = 2). Each of these lesions was a low-grade glioma histologically and each remained stable in size after treatment (median follow-up = 4.25 years). Four patients with tectal tumors underwent insertion of a CSF shunt for hydrocephalus, but required no specific treatment for the tumor. None of the patients with diffuse brainstem lesions or focal areas of hypointensity required any intervention for the tumor. All 21 patients are presently alive and well. We conclude that the biological behavior of brainstem lesions in patients with NF1 differs significantly from that of lesions with a similar appearance in patients without this disorder. Although these lesions may at some time in their course exhibit clinical and radiographic progression, most do not require specific intervention. The lesions that are most likely to progress and require therapy are focal enhancing tumors; however, even lesions in this subgroup may stabilize in size or regress spontaneously without intervention. Based on these results, we recommend that intervention be limited to those lesions that exhibit rapid or unrelenting growth on serial images or that produce significant clinical deterioration.
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PMID:The management of brainstem gliomas in patients with neurofibromatosis 1. 864 65


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