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)

A multicenter phase I-II trial of intravenous (IV) human recombinant interferon beta (rIFN-beta; Betaseron; Triton Bioscience Inc, Almeda, CA) was conducted in children with recurrent or progressive primary brain and spinal cord tumors. A total of 29 patients were enrolled: high-grade astrocytoma (12), brainstem glioma (nine), and primitive neuroectadermal tumor (three), ependymoma (two), germ cell (two), and spinal cord astrocytoma (one). Betaseron was given by IV infusion over 30 minutes 3 times per week (Monday-Wednesday-Friday [MWF]). Four dose levels were studied, and at least three patients were entered at each dose level. The treatment plan began with a three-step dose escalation for each patient over 6 weeks (initiation phase). The dose-escalation schema for the four dose levels was: 50-100-200, 100-200-400, 200-300-500, and 300-400-600 x 10(6) (M) IU/m2. Patients experiencing an objective response or stable disease after 6 weeks entered the maintenance phase at the final escalated dose, ie, 200, 400, 500, or 600 mlU/m2 (MWF). Common transient effects included chills, fever, and fatigue. Dose-limiting toxicities were hematologic, hepatic, and CNS. The maintenance maximum-tolerable dose (MTD) was 500 mlU/m2, ie, dose level 3. Response was assessed at completion of the initiation phase and at 2-month intervals during the maintenance phase. Objective partial responses were seen in patients with high-grade astrocytoma (two) and brain-stem glioma (two). Thus, four of 21 (19%) assessable patients had partial responses for a median of 4 months. Eight patients had stable disease for a median of 5+ (2 to 14+) months. Antineoplastic activity has been identified in children with high-grade astrocytomas and brainstem gliomas in a dose-intensive regimen.
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PMID:Recombinant interferon beta: a phase I-II trial in children with recurrent brain tumors. 201 20

The effects of radiation therapy on 29 brain stem gliomas in childhood were evaluated by computed tomography (CT). The patients received radiation of 2 Gy/day as a single fraction, 5 day a week with a total dose of 40 to 60 Gy. Initial CT findings of brain stem gliomas were divided into two types: diffuse and localized. Of 29 children, 5 had localized and 24 had diffuse tumor. Histological diagnoses were available for 18 patients, 4 with localized and 14 with diffuse tumor. All of the localized tumors were astrocytomas and diffuse tumors included 13 anaplastic gliomas (glioblastomas), 3 anaplastic astrocytomas, and one astrocytoma. Complete response or partial response to radiation therapy was observed on CT in 100% (5/5) of the localized tumors and 46% (11/13) of the diffuse tumors at the first evaluation. Contrary to expectation, low-grade gliomas responded much better to radiation therapy than high-grade gliomas. The response rates were 80% (4/5) in astrocytoma, 67% (2/3) in anaplastic astrocytoma, and 38% (5/13) in anaplastic glioma. In the follow-up CT after radiation therapy, a delayed effect was observed in only one of the 24 diffuse tumors. Nine of 10 children who had a re-irradiation following the recurrence experienced very little benefit. None of the patients with localized tumors have shown evidence of tumor progression or recurrence, and the quality of their life has been excellent. On the other hand, all of the patients with diffuse tumor died within 20 months after initial treatment. The results of this study suggest that radiation therapy is beneficial for localized tumors but not for diffuse tumors, and new treatments need to be developed for diffuse tumors.
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PMID:[Evaluation of radiation therapy in pediatric brain stem glioma by computed tomography: CT findings and tumor response to radiotherapy]. 202 68

Magnetic resonance imaging has been used increasingly in the staging and evaluation of neoplasia of the brain and leptomeninges. In the classification of gliomas, the MR accuracy rate approaches that of pathologic diagnosis. Contrast-enhanced MR imaging has improved specificity in evaluating brain tumors in children and is now the preferred modality for evaluating leptomeningeal metastases of the brain and spine. MR imaging in children has also increased the specificity of histologic diagnosis in hypothalamic hamartoma and juvenile pilocytic astrocytoma. Gadolinium enhancement is most useful in patients older than 35 years of age who have focal neurologic complaints and certain disease histories. The expense of gadolinium contrast material is the major drawback to its routine use. In patients with seizure disorder, MR imaging is more sensitive than CT for detecting abnormalities such as mesial temporal sclerosis, tumors, and vascular malformations. Gadolinium enhancement may be useful in differentiating tumors from mesial temporal sclerosis. Recent reports on the use of MR spectroscopy for evaluating brain metabolism and tumors demonstrate that differences in metabolites exist. A correlation was found in epidermoid tumors between high signal on T1-weighted images and high lipid content, and several studies have shown a positive correlation between glioma grade and glycolytic activity as determined on 18F-2-fluoro-2-deoxy-D-glucose positron emission tomography.
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PMID:Imaging of central nervous system tumors. 202 6

In this study, we have investigated the expression of the neural cell adhesion molecule (NCAM) in the human brain, primary brain tumours and neuroblastoma. Adult brain was found to express discrete isoforms of 180, 170, 140 and 120 kDa, which on neuraminidase treatment resolved into bands of 180, 170, 140, 120 and 95 kDa. Primary brain tumours such as Schwannoma and medulloblastoma expressed embryonic NCAM characterised by a high level of glycosylation, whereas other tumours, e.g. astrocytoma, meningioma, glioma and oligodendroglioma expressed adult NCAM. Post-neuraminidase treatment, differential expression of the 180, 170, 140, 120 and 95 kDa isoforms were noted in these various tumour types. On the other hand, neuroblastoma cell lines were found to express only embryonic NCAM, which after neuraminidase treatment resulted in differential presence of only 180, 140 and 120 kDa proteins.
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PMID:Expression of the cluster 1 antigen (neural cell adhesion molecule) in neuroectodermal tumours. 203 10

In an attempt to define the angiotensin II receptor subtype responsible for prostaglandin release, we studied the effects of the nonpeptide, subtype 1 (or B) selective angiotensin II antagonist, DuP 753. Release of prostaglandin E2 produced by angiotensin II from rat C6 glioma, human astrocytoma, or porcine aortic smooth muscle cells in culture was blocked by the addition of the 10(-7) M of DuP 753. In contrast, the release of prostacyclin, as assessed by measurement of the stable metabolite 6-keto PGF1 alpha, was not attenuated by addition of Du P 753. However, DuP 753 either alone or in combination with angiotensin II, produced dose-dependent increases in prostacyclin release with doses as low as 10(-8) M. In the absence of angiotensin II, DuP 753 also increased prostaglandin E2 release at high doses but the magnitude of the potentiation was substantially less than for prostacyclin release (50 to 250% v 400 to 2800% above basal). Thus, we clearly show that angiotensin II stimulates PGE2 release via subtype 1 (or B) angiotensin receptors. Whether the effect of DuP 753 on prostaglandin release is a result of agonistic properties or intrinsic effects unrelated to blockage of angiotensin II receptors remains to be determined. The marked stimulatory effect of DuP 753 release precludes characterization of the receptor subtype that mediates the Ang II-induced release of prostacyclin. Nonetheless, potent stimulation of prostacyclin release by DuP 753, especially in vascular smooth muscle cells, requires reevaluation of the mechanisms that participate in the anti-hypertensive effects of the compound.
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PMID:The nonpeptide angiotensin II antagonist DuP 753 is a potent stimulus for prostacyclin synthesis. 204 99

In this study we investigated the ultrastructure of human glioma capillaries in operated sample of low grade astrocytomas and malignant gliomas. Electronmicrographs of a total of 58 vessels were analyzed with computer assisted morphometry for ultrastructural evidence of permeability routes. All of these vessels were present in the marginal area of tumors devoid of necrosis, less than 10 micron in diameter and containing one nucleus at least on axial section. We found that: (1) The number of pinocytic vesicles was significantly higher in capillaries from malignant glioma (an average of 8.1 per 1 micron (2) cytoplasm) than those from low grade astrocytoma (an average of 4.0 per 1 micron (2) cytoplasm). In capillaries from malignant glioma, most of the pinocytic vesicles were arranged in the abluminal side of endothelium and some of them were fused each other. (2) Abnormal endothelial intercellular junctions which were defined as short tight junctions (less than or equal to 0.25 microns) were equally but infrequently seen in low grade astrocytomas and malignant gliomas. (3) Fenestrations in the endothelium were not seen. Therefore we suggest that the high vascular permeability and resultant brain edema in malignant gliomas is likely to increased pinocytic vesicles and rare but abnormal inter endothelial junctions.
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PMID:[Ultrastructure of glioma vessel--morphometric study for vascular permeability]. 205 22

Radiolabelled monoclonal antibodies (131I-MUC 8-22, 131I-MUC 2-63) were used for external scintigraphy of human glioma xenografts. To induce transplantation tumors. 5 x 10(6) cells (85HG-66) of an in vitro established human malignant astrocytoma (N66/85) were inoculated s.c. in BALB/c-nu/nu mice. The labelling of the immunoglobulins with 131iodine was carried out according to the iodogen method, the nude mice, bearing xenograft, received 30 m. 131I-labelled intact monoclonal immunoglobulins (200mCi: 7,4MBq) and the imaging was performed on days 4, 8 and 12 after the application. After 4 days, a clear tumor accumulation of iodinated MUC 2-63 antibodies recognizing surface determinants was visible. This enrichment of monoclonal antibodies (MAbs) led to a characteristic tumor presentation on day 8. Obviously, the MUC 2-63 antibodies remain in the tumor tissue for a long time, so that even on day 12 satisfactory tumor imaging is possible. On the other hand, neither with normal mouse IgG nor with MUC 8-22 antibodies - which react with intracellular structures - could a tumor localization be achieved. The result of the studies on the distribution of 131I-MUC 2-63 on day 19 was that the activity in the tumor tissue was about 4.4 times higher than in the blood and even more times higher than in solid organs.
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PMID:Radioimmunodetection of human glioma xenografts by radiolabelled monoclonal antibodies. 206 9

Contradictory results have been reported claiming either none, partial or almost complete correlation between the complexity of GSL compound profiles and the assumed glial tumor differentiation. Therefore an attempt was made to compare GSL patterns with both the general (final) tumor diagnosis and malignancy grade (WHO) as well as the regional evaluation of the histology and the grading in the tumor tissue pieces directly subjected to biochemical analysis. Regional and general (final) diagnosis did not always correspond, especially when more than one tissue sample of a given tumor was analyzed. Four GSL component patterns were identified by TLC: GSL-type I with gangliosides primarily of the simple Glac-family lacking sulfatide and the more complex Gtri- and Gtet-gangliosides, GSL-type II with ganglioside of the Glac- and Gtri-families, also without sulfatide, and GSL-type III, with more complex gangliosides of the Gtri- and Gtet-families in addition to Glac-gangliosides and sulfatide, similar to the normal brain pattern, and the pattern of normal brain. There was only insufficient correlation between these GSL-type patterns and final diagnoses. However, between regional diagnosis of astrocytoma II and GSL-type III on the one hand and glioblastoma multiforme IV and GSL-type I on the other hand, a coincidence of more than 85% was found. In only 50% the intermediate GSL-type II and glioma III were associated. There was no relation between GFAP or vimentin expression and histology or GSL-type both with regard to final and regional diagnoses. Regional astrocytoma architectures exhibiting GSL-type III were mostly fibrillary, whilst glioblastomas with GSL component pattern I had often a giant cell make up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tissue architecture and glycosphingolipid content in human gliomas II-IV. 206 94

The changes of cerebral blood flow (CBF) and metabolism of normal brain tissue after surgery, radiation, and chemotherapy in brain tumor patients were measured by positron emission tomography (PET). The subjects consisted of 6 men and 3 women, and were from 11 to 62 years old. Those were four patients with glioblastomas, one patient with malignant oligodendroglioma, one patient with astrocytoma grade II, one patient with astrocytoma grade III, one patient with pontine glioma, one patient with pineal germinoma. Seven patients were operated and pathohistologically diagnosed. Two patients with pineal germinoma and pontine glioma were not operated and radiologically diagnosed. Of 7 operated patients, first PET was performed before operation in 3 patients, and from 10 to 16 days after operation in 4 patients. Following first PET, the patients were treated with irradiation (1 case), or with both irradiation and chemotherapy (8 cases). The total radiation dose for tumor was from 59 to 61 Gy distributed in a period of 6-8 weeks. Whole brain irradiation was performed up to 30 or 40 Gy, with a remaining dosimetry (20-30 Gy focused on the tumor field. Chemotherapy consisted of intravenous administration of ACNU and oral administration of FT-207. Second PET was performed 1 month after therapy (9 cases), and third PET was performed from 4 to 24 months after therapy (6 cases). Fourth PET was performed in 2 patients (22 and 35 months after therapy), and fifth PET was performed in one patient (35 months after therapy).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The changes of cerebral blood flow and metabolism of normal brain tissue after surgery, radiation, and chemotherapy in brain tumor patients: evaluated by position emission tomography]. 207 54

In the process of malignant transformation, astrocytoma cells display a number of surface antigens not expressed by their normal adult counterparts and which have been identified by monoclonal antibodies and characterized biochemically. These include tumor associated antigens (TAA) such as oncofetal antigens of neuroectodermal origin or oncogene products such as epitopes in the extracellular domain of the epidermal growth factor receptor, as well as major histocompatibility antigens (MHC) of class I and class II. Glioma cells also secrete lymphokines like IL-1 and IL-6. The concomitant expression of TAA and MHC together with the disruption of the blood brain barrier may elicit a humoral or cell mediated immune response from the tumor bearing host as demonstrated by the functional analysis of tumor infiltrating lymphocytes. However this response is extremely weak and obviously inefficient because the tumor cells secrete factors which can inhibit or completely abrogate the immune attack by cytotoxic T cells. Among these factors, TGF-beta 2 and PGE2 are of particular interest since they may explain the generally depressed cellular immune response observed in patients with malignant gliomas. To be efficient any form of immunotherapy will require abatement of these suppressive activities in addition to stimulation of the effector functions.
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PMID:Immunotherapy of brain tumors. 209 5


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