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 report presents a seven-week old girl suffering from signs of raised ICP. A ventriculo-atrial shunt was inserted and replaced by a ventriculo-abdominal shunt due to occlusion at 15 months of age. At 16 months, craniotomy and resection of an oligodendroglioma was performed and the shunt was preserved. The child died at 18 months due to extensive local recurrence. Autopsy revealed massive peritoneal metastases of the tumor. This is the eleventh published case of canalicular metastases of glioma.
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PMID:[Extraneural metastasis of an oligodendroglioma in ventriculo-peritoneal shunt]. 36 90

Sequential MR imaging with gadolinium-diethylenetriaminepentaacetic acid (Gd-DTPA) and sequential measurements of plasma Gd-DTPA concentration by inductively coupled plasma atomic emission spectroscopy (ICP-AES) were used to estimate the blood-to-tissue transport coefficient (Ki) in the 36B-10 rat glioma model. For these measurements, tissue Gd-DTPA concentration was estimated from tumor enhancement by correlation with calibration measurements obtained by ICP-AES analysis of tumor tissue. The 14 animals for which Ki was calculated can be grouped into those imaged at 11 days following tumor implantation, at 13-18 days, and at 20 days. The mean (+SEM) Ki values for these groups were 1.1 + 0.24, 9.2 + 0.8, and 13.4 + 1.7 ml/kg-min, respectively. These results correspond well with published data obtained by quantitative autoradiography. It is concluded that frequent sequential imaging and a graphical approach to Ki calculation are promising methods for determining the blood-to-tissue transport coefficient noninvasively by contrast-enhanced MRI.
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PMID:Measurement of blood-brain barrier permeability in a tumor model using magnetic resonance imaging with gadolinium-DTPA. 143 11

Secondary mediator compounds are postulated to have a role in vasogenic oedematogenesis. They may also cause focal brain dysfunction due to their neuronal, axonal and glial modulating properties. Using the feline model of infusion brain oedema the effects of right frontal intracerebral infusion (200 microliters/hr for 3 hrs) of saline, bradykinin (10(-4) to 10(-6) M), arachidonic acid (10(-2) to 10(-3) M), 20% protein and four human glioma cyst fluids were evaluated. Somatosensory evoked potentials (SSEP), motor evoked potentials (MEPs), rCBF and rCBF CO2 reactivity (Hydrogen clearance). ICP, craniospinal compliance, local brain tissue water content (microgravimety), brain histology and BBB function (Evans Blue 2%) were measured. Brain water content increased locally from 69% to 79%, ICP increased (by mean 14 mmHg) and compliance decreased (mean 70%) and there were the histological features of brain oedema with all infusates. BBB opening occurred with Bradykinin (+), arachidonic acid (++), 20% protein ( ) and glioma cyst fluid (4+). Polymorphic and macrophage infiltrates were seen with all infusions but rCBF and MEPs remained normal. SSEPs changed with high dose bradykinin and some glioma cyst infusates whilst CBF CO2 reactivity was locally impaired by all infusates except saline and arachidonic acid. This study suggests that certain compounds in brain oedema fluid could mediate local brain dysfunction.
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PMID:The contribution of secondary mediators to the etiology and pathophysiology of brain oedema: studies using a feline infusion oedema model. 212 86

The toxicity and binding of the three new carborane based compounds: 2 (1,2-dicarba-closo-dodecaborane (12)-1(-yl-methoxy)-2-(3-amino-propyl))-1,3-propanediol, called DAC-1; 7-(3-amino-propyl)-7,8-dicarba-nido-undecarborate (-1) called ANC-1; and rac-1-(9-o-carboranyl)-nonyl-2-methyl-glycero-3- phosphocholine, called B-Et-11-OMe, were analyzed with cultured human glioma cells, U-343MGa, and mouse melanoma cells, B16, as biological models. The previously developed compound di-sodium undecahydro-mercapto-closo-dodecarborate (BSH), which is tested for therapy of malignant gliomas, was analyzed for comparison. In the toxicity tests the cells were exposed to the substances at cell culture medium concentrations in the range 0-50 ppm boron for 1 or 20 h and thereafter analyzed regarding growth. Growth-disturbing effects were seen for the two compounds DAC-1 and B-Et-11-OMe at the concentrations corresponding to 15 and 50 ppm boron, respectively. The compounds ANC-1 and BSH showed no growth-disturbing effects at the tested concentrations. In the binding tests, the cells were incubated for 20 h at about the highest compound concentrations that did not cause growth disturbances. The boron content in the cells was then determined by inductively coupled plasma-atomic emission spectrometry (ICP-AES) and in some cases ICP-mass spectrometry (ICP-MS). The most extensive binding was seen for DAC-1 and B-Et-11-OMe, which accumulated boron to about 100 and 60 times, respectively, compared with the concentration in the culture medium. The compound ANC-1 also accumulated boron in the cells but the boron could be easily washed out indicating no or only a weak binding. BSH did not accumulate. Further analysis should be made regarding biological properties such as intracellular compartmentalization, metabolic interference and tumor specificity of the compounds DAC-1 and B-Et-11-OMe.
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PMID:New carborane-based compounds for boron neutron capture therapy: binding and toxicity of ANC-1, DAC-1 and B-Et-11-OMe in cultured human glioma and mouse melanoma cells. 818 29

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

Preoperative treatment with glucocorticoids in patients with an intracranial tumour has been neurosurgical practice for more than 30 years. Recently, however, a less beneficial effect in patients with a meningeoma is reported. This study included 4 patients with a glioma, 4 with a metastasis and 5 with a meningeoma. All patients had a substantial amount of oedema. The effect of methylprednisolone was monitored during 5 days by clinical examination and epidural pressure measurement. ICP reduction was found in 4 of 13 patients. All observations of decreasing pressure were in patients with a malignant tumour and an initial ICP > 15 mmHg. All 4 patients improved clinically. Another 4 patients with a benign meningioma had a significant increase of ICP and none of them experienced clinical improvement. Clinical deterioration was not observed in any patient despite increasing ICP in some cases. In summary, a beneficial effect of GC was demonstrated only in patients with a malignant tumour and augmented pre-treatment ICP.
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PMID:Effect of glucocorticoids on ICP in patients with a cerebral tumour. 930 70

The objective of the present study was to construct epidermal growth factor receptor (EGFR) targeting cetuximab-immunoliposomes (ILs) for targeted delivery of boron compounds to EGFR(+) glioma cells for neutron capture therapy. The ILs were synthesized by using a novel cholesterol-based membrane anchor, maleimido-PEG-cholesterol (Mal-PEG-Chol), to incorporate cetuximab into liposomes by either surface conjugation or a post-insertion method. For post-insertion, the transfer efficiency of MAb conjugates from micelles to liposome was examined at varying temperatures, mPEG2000-DSPE ratios, and micelle-to-liposome lipid ratios. Following this, the cetuximab-ILs were evaluated for targeted delivery of the encapsulated boron anion, dodecahydro-closo-dodecaborate (2-) (B12H122-), to human EGFR gene transfected F98EGFR glioma cells as potential delivery agents for boron neutron capture therapy (BNCT). In addition, cellular uptake of cetuximab-ILs, encapsulating a fluorescence dye, was analyzed by confocal fluorescence microscopy and flow cytometry, and boron content was quantified by ICP-MS. Much greater ( approximately 8-fold) cellular uptake of boron was obtained using cetuximab-ILs in EGFR(+) F98EGFR compared with nontargeted human IgG-ILs. On the basis of these observations, we have concluded that cholesterol can serve as an effective anchor for MAb in liposomes, and cetuximab-ILs are potentially useful delivery vehicles for BNCT of gliomas.
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PMID:Synthesis of cetuximab-immunoliposomes via a cholesterol-based membrane anchor for targeting of EGFR. 1722 62

The over-expression of sialic acid on the surface of cancer cells compared with normal ones makes this nine-carbon sugar an attractive biomarker for molecular diagnosis and therapy. Here, we describe a study on the molecular recognition of sialic acid end groups on the surface of human glioma cells by (160)Tb-DTPA-EN(2), (160)Tb-DTPA-(ENPBA)(2) and (160)Tb-DTPA-(PBA)(2) complexes. The results show Tb-DTPA-(ENPBA)(2) to be the most efficient targeting agent, due to the electrostatic interaction between its two positively charged ammonium groups and the negatively charged cell surface, which provides an additional stabilization of the covalent binding through the PBA moieties and the sialic acid diol functions. Up to 5.5 nmol Tb/mg protein is taken up by the cells. ICP analysis after incubation experiments with non-radioactive Tb-DTPA-(ENPBA)(2) suggests that dissociation of Tb from this complex occurs after its binding to the cell surface. Most likely, most of the free Tb remains adsorbed on the surface of the cells, although internalization of a small amount cannot be excluded.
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PMID:Phenylboronate 160Tb complexes for molecular recognition of glycoproteins expressed on tumor cells. 1730 40

The duration of cisplatin release from most of the drug delivery devices seemed to be shorter than 14 days except large microparticles. The objective of this study was to fabricate and characterize cisplatin-loaded PLA microparticles, PLA/PLGA (30/70) composite microparticles, and fibers as formulations for long-term sustained delivery of cisplatin to treat C6 glioma in vitro by electrospray and electrospinning techniques. Cisplatin-loaded biodegradable microparticles with particle size of around 5 microm and fiber fabrics with diameter of 0.5-1.7 microm were obtained using electrospray and electrospinning techniques. Encapsulation efficiency and in vitro release of formulations were measured by ICP-OES. The encapsulation efficiency for different samples of microparticles was approximately from 33% to 72% and the fiber fabrics had encapsulation efficiency greater than 90%. Cisplatin-loaded microparticles showed typical characteristics of cisplatin release profile: a large initial burst followed by a sustained slow release of 35 days. The composite PLA/PLGA (30/70) microparticles could reduce the initial burst release of cisplatin because of their core-shell structures. In contrast, more than 75 days sustained release could be achieved by fiber fabric formulations without large initial burst. MTT assay was used to quantify the cytotoxicity of different formulations against C6 glioma cells. Microparticle formulations had slightly higher cytotoxicity than free drug. In contrast, the cytotoxicity of fiber fabrics formulation was around 4 times higher than of the free drug based on the actual amount of drug released. The microparticle and fiber fabric formulations presented may be promising for the sustained delivery of cisplatin to eliminate the undesired side effects caused by direct injection of cisplatin solution in systemic administration.
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PMID:Biodegradable microparticles and fiber fabrics for sustained delivery of cisplatin to treat C6 glioma in vitro. 1789 69

The present study reports the synthesis of a novel compound with the formula [Ru(2)(aGLA)4Cl] according to elemental analyses data, referred to as Ru(2)GLA. The electronic spectra of Ru(2)GLA is typical of a mixed valent diruthenium(II,III) carboxylate. Ru(2)GLA was synthesized with the aim of combining and possibly improving the anti-tumour properties of the two active components ruthenium and gamma-linolenic acid (GLA). The properties of Ru(2)GLA were tested in C6 rat glioma cells by analysing cell number, viability, lipid droplet formation, apoptosis, cell cycle distribution, mitochondrial membrane potential and reactive oxygen species. Ru(2)GLA inhibited cell proliferation in a time and concentration dependent manner. Nile Red staining suggested that Ru(2)GLA enters the cells and ICP-AES elemental analysis found an increase in ruthenium from <0.02 to 425 mg/Kg in treated cells. The sub-G1 apoptotic cell population was increased by Ru(2)GLA (22 +/- 5.2%) when analysed by FACS and this was confirmed by Hoechst staining of nuclei. Mitochondrial membrane potential was decreased in the presence of Ru(2)GLA (44 +/- 2.3%). In contrast, the cells which maintained a high mitochondrial membrane potential had an increase (18 +/- 1.5%) in reactive oxygen species generation. Both decreased mitochondrial membrane potential and increased reactive oxygen species generation may be involved in triggering apoptosis in Ru(2)GLA exposed cells. The EC(50) for Ru(2)GLA decreased with increasing time of exposure from 285 microM at 24 h, 211 microM at 48 h to 81 microM at 72 h. In conclusion, Ru(2)GLA is a novel drug with antiproliferative properties in C6 glioma cells and is a potential candidate for novel therapies in gliomas.
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PMID:The novel ruthenium-gamma-linolenic complex [Ru(2)(aGLA)(4)Cl] inhibits C6 rat glioma cell proliferation and induces changes in mitochondrial membrane potential, increased reactive oxygen species generation and apoptosis in vitro. 1992 75


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