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)

Photodynamic therapy is a binary treatment combining the selective uptake of a photosensitizer into a tumour followed by irradiation of the tumour with light of the appropriate wavelength to cause activation of the sensitizer as selective tumour kill. Photodynamic therapy has been extensively investigated in laboratory studies in the treatment of cerebral tumours and has been utilised in clinical trials to treat a variety of tumours including cerebral glioma. The clinical trials have usually used PDT as an adjuvant therapy following tumour resection but studies are being undertaken to use the treatment in combination with stereotactic techniques. The photosensitizer haematoporphyrin derivative (HpD) has been shown to be selectively localised into all grades of glioma with a direct correlation between the grade of glioma and HpD level in the tumour. The levels were highest in the glioblastoma multiforme (mean uptake of 5.9 micrograms HpD/g tumour wet weight) and lower in the intermediate grade anaplastic astrocytoma (2.4 micrograms/g) and low grade astrocytoma (1.6 micrograms/g). Uptake into normal brain tissue taken from HpD sensitized patients was 0.2 microgram/g. HpD was also localised into the brain adjacent to the tumour region.
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PMID:Photodynamic therapy of brain tumours. 821 3

In this paper we present a case of glioma which was located in the cerebellopontine angle. The patient, a 3-year-old male, experienced difficulty with gait for one month before admission. He was admitted to Toyota Memorial Hospital on February 2, 1991, suffering from severe headache and vomiting. Neurological examination upon admission revealed horizontal nystagmus and ataxia. MRI revealed a mass in the cerebellopontine angle. Craniotomy was performed on February 4, 1991, and a tumor was revealed in the cerebellopontine angle. The tumor was clearly demarcated and encapsulated; the cerebellum and brainstem were compressed without damage. Most of the tumor was removed. A histopathological summary of the tumor follows. The tumor appeared as exophytic lesions on the pons, extending into the cerebellopontine angle. Tumor cells contained small round nuclei and acidophilic cytoplasm. The oncocyte, which was growing endomorphically, revealed a short-cell projection, suggesting a tendency to penetrate blood vessels. Intercellular microcystic degeneration was observed clearly, with some parts of the oncocyte forming a myxoid matrix. Immunohistochemically, most of the tumor cells reacted positively to Vimentin, but negatively to S-100 protein and GFAP. Given the pathological information, the tumor was interpreted as anaplastic astrocytoma. Postoperative radiation therapy was performed, but the patient died four months later because the tumor had spread to the brainstem. In this paper we discuss the differential diagnosis of the cerebellopontine angle tumor and the appearance of anaplastic astrocytoma as exophytic lesions on the pons and the spread of the tumor into the cerebellopontine angle.
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PMID:Anaplastic astrocytoma in the cerebellopontine angle. 822 Jul 82

The objective of our study was to determine the frequency of EGF-receptor-gene rearrangement in relation to tumour-growth behaviour in an unselected group of glioma patients. We investigated 73 glial tumours with different grades of malignancy (17 low-grade gliomas, 14 anaplastic variants, and 42 GBM) by Southern analysis, reverse transcriptase PCR (RT-PCR) amplification of mRNA, and Western analysis. An amplification of the EGF-receptor gene was present in 19/42 GBM but in only 1 anaplastic astrocytoma. By RT-PCR, 4/19 GBM with gene amplification showed a specific amino-terminal aberrant splice mutation of 801 bp in addition to undeleted mRNA. By Western analysis, 27/42 GBM showed expression of the EGF-receptor protein. Protein levels, however, varied among individual tumours. Four GBM containing an aberrant splice mutation exhibited an immunoreactive protein of 130 kDa MW in addition to the normal EGF-receptor protein p170. All GBM patients underwent surgery followed by a standard course of radiotherapy. Neuroradiological follow-up in 31/42 GBM patients consisted of bimonthly MRI examinations. There was a statistically significant difference in the mean latency period until tumour regrowth of patients suffering from GBM with and without EGF-receptor-gene amplification (9 weeks vs. 32 weeks). Our data indicate more rapid tumour regrowth kinetics of GBM with amplified EGF receptor genes in vivo.
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PMID:Amplification of the epidermal-growth-factor-receptor gene correlates with different growth behaviour in human glioblastoma. 826 81

We reported a multicentric glioma having three separate lesions in the cerebrum. A 75-year old man was hospitalized with progressive disorientation. Computed tomography demonstrated two lesions in the left temporal lobe and the right frontal lobe. Magnetic resonance image disclosed one more lesion in the right occipital lobe. 2-staged operative procedures were performed for the left temporal and the right frontal tumors. It was histologically proven that one was glioblastoma and the other was anaplastic astrocytoma. The patient subsequently underwent radiotherapy and chemotherapy. Most multicentric gliomas are diagnosed in autopsy. Therefore it should be stressed that diagnosis is best made by biopsy or surgery. We discussed what therapy we should use for this fatal disease.
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PMID:[A multicentric glioma exhibiting three supratentorial lesions]. 829 8

Between January 1983 and November 1987, the Radiation Therapy Oncology Group conducted a prospective, randomized, multi-institutional, dose searching Phase I/II trial to evaluate hyperfractionated radiation therapy in the treatment of supratentorial malignant glioma. Patients with anaplastic astrocytoma, or glioblastoma multiforme, age 18-70 years with a Karnofsky performance status of 40-100 were stratified according to age, Karnofsky performance status, and histology, and were randomized. Initially randomization was to one of three arms: 64.8 Gy, 72.0 Gy, and 76.8 Gy. Fractions of 1.2 Gy were given twice daily, 5 days per week, with intervals of 4 to 8 hr. All patients received bis-chlorethyl nitrosourea (BCNU) 80 mg/m2 on days 3, 4, 5 of radiation therapy and then every 8 weeks for 1 year. After acceptable rates of acute and late effects were found, the randomization was changed to 81.6 Gy and 72.0 Gy with a weighting of 2:1. Out of 466 patients randomized, 435 were analyzed. The distribution of prognostic factors was comparable among the 76.8 Gy arm, 81.6 Gy arm, and the final randomization of the 72 Gy arm. The 64.8 Gy arm and the initial randomization of the 72 Gy arm had somewhat worse prognostic variables. Late radiation toxicity occurred in 1.3-6.8% of the patients, with a modest increase with increasing radiation dose. The best survival occurred in those patients treated with 72 Gy (median survival of 12.8 months overall, and 14 months for the final 72 Gy randomization). The Cox proportional hazards model confirmed the prognostic variables of age, histology and Karnofsky performance status. In addition, the longer interval of 4.5-8 hr was associated with a worse prognosis than the 4-4.4 hr interval (p = 0.0011). The difference in survival between the 81.6 Gy arm and the lower three arms approached significance (p = 0.078) with inferior survival observed in the 81.6 Gy arm. When therapy was evaluated by radiation therapy dose received (60-74.4 Gy compared with 74.5-84.0 Gy), the p value was 0.062 in favor of the lower dose range. Patients with anaplastic astrocytoma treated with 72 Gy by hyperfractionation + BCNU had at least as good a survival as those treated with 60 Gy by conventional fractionation + BCNU on Radiation Therapy Oncology Group protocols 7401 and 7918. This suggests that 72 Gy delivered by 1.2 Gy twice daily is no more toxic than 60 Gy delivered by conventional fractionation.
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PMID:Hyperfractionated radiation therapy and bis-chlorethyl nitrosourea in the treatment of malignant glioma--possible advantage observed at 72.0 Gy in 1.2 Gy B.I.D. fractions: report of the Radiation Therapy Oncology Group Protocol 8302. 838 May 67

Mean survival of patients with malignant glioma is six months. Only 7.5% of these patients survive two years. We identified 14 patients, nine with glioblastoma multiforme and five with anaplastic astrocytoma, who survived more than two years. All were treated initially with surgery, radiation and adjuvant chemotherapy. One patient who received three years of nitrosourea has lived longer than 7.3 years. Seven of the 14 patients have no sign of tumor recurrence four years after diagnosis. Nine surviving patients were younger than 45 years of age at the time of diagnosis. Five died of tumor recurrence with the median survival time of 3.5 years. This data suggests that onset at a younger age (< 45 years), multimodality therapy, high Karnofsky Performance Scale and frontal lobe tumors were the major prognostic factors that contributed to long-term survival.
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PMID:Long-term survival in malignant glioma. Prognostic factors. 838 66

Expression of the human placental form of glutathione S-transferase (GST-pi) in pediatric gliomas, consisting of three pilocytic astrocytomas (grade 1), two fibrillary astrocytomas (grade 2), three anaplastic astrocytomas (grade 3), and one glioblastoma multiforme (grade 4), were investigated by immunohistochemical methods. Western blot analysis for GST-pi using proteins extracted from formalin-fixed and paraffin-embedded glioma specimens was performed and compared with the results of immunohistochemistry. Both the immunohistochemical examination and the Western blot analysis of pediatric gliomas revealed that malignant gliomas such as anaplastic astrocytoma and glioblastoma had strong expression of GST-pi while benign gliomas showed weak GST-pi expression.
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PMID:Expression of the placental form of glutathione S-transferase in pediatric gliomas. 839 67

p16 is involved in a cell cycle regulatory cascade that includes cyclin-dependent kinase 4 (cdk4), cyclin D1, and pRb (retinoblastoma). Alterations of each of these components have been described in primary human glioblastoma multiforme (GBM) or in GBM cell lines. Because perturbation of any component in this pathway may have similar oncogenic effects, we studied the relationship between abnormalities of CDKN2/p16 and RB, the two commonly involved tumor suppressor genes, in 55 astrocytic gliomas (42 GBMs, 8 anaplastic astrocytomas, and 5 astrocytomas). By using comparative multiplex PCR, homozygous deletions of the CDKN2/p16 gene were detected in 24 GBMs (57%) and in 2 anaplastic astrocytomas. Two additional GBMs and one anaplastic astrocytoma had allelic loss of chromosome 9p, as assessed by microsatellite polymorphisms flanking the CDKN2/p16 region. Single-strand conformation polymorphism and DNA sequencing analysis of all three coding exons of CDKN2/p16 revealed a frameshift mutation (four-bp deletion) in one of the three GBMs that had lost the remaining 9p allele. Allelic loss of chromosome 13q at the RB gene, RB gene mutations, or loss of pRb expression was noted in 14 GBMs (33%) and 2 anaplastic astrocytomas. Thirty-six of 42 GBMs (86%) had alterations of either CDKN2/p16 (n = 22), RB (n = 10), or both (n = 4); these two genetic changes, however, were relatively exclusive (P = 0.003). Furthermore, of the six GBMs without either CDKN2/p16 or RB gene abnormalities, one case had CDK4 gene amplification. These data indicate that the vast majority of GBMs probably have inactivation of the p16-cdk4/cyclin D1-pRb pathway. The findings also provide corroborative evidence that CDKN2/p16 and RB are the critical glioma tumor suppressor genes on chromosomes 9p and 13q, respectively.
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PMID:CDKN2/p16 or RB alterations occur in the majority of glioblastomas and are inversely correlated. 854 55

Between February 1993 and March 1994, 75 metastases, 16 gliomas and 2 AIDS-related malignant lymphomas were treated with Gamma Knife radiosurgery. Metastatic brain tumors (54% lung cancer, 14% breast cancer, 13.5% melanoma) were the most frequent and clinically rewarding cases. So-called local control was achieved in almost all patients, the vast majority showing neurological improvement associated with radiological disappearance or dramatic shrinkage of the tumor within 9-12 weeks from treatment. According to our modified 'Pittsburgh' protocol, we have treated up to four distinct intracranial lesions, up to a total maximum volume of 20 cm3, with an average surface dose of 25 Gy, with or without additional whole brain radiotherapy (WBR). Preliminary follow-up data seem to confirm increased quality of life and survival rates. The results were particularly striking whenever primary tumors were under control, and were poorly influenced by associated WBR. Gamma Knife treatment was also performed in a selected group of patients with small-to-medium-sized, well-defined, histologically proven, cerebral gliomas. The main indications for radiosurgery were high-risk surgery, multifocal disease, ventricular seeding and unresected or recurrent tumor. The prescription doses ranged from 18 to 30 Gy, with a mean of 27 Gy. Low-grade astrocytomas (9/16 cases) showed the better clinical and radiological response to treatment, with neurological recovery and significant reduction in tumor volume within 3-5 months in 5 of the 9 patients. In 4 of 7 high-grade gliomas, there was little or no response. However, an impressive radiological regression with full clinical recovery was observed in 2 high-grade cases with small tumor volumes: a recurrent, anaplastic 'mixed glioma' of the pineal region and a double ventricular seeding of a previously operated anaplastic astrocytoma.
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PMID:Gamma Knife radiosurgery of primary and metastatic malignant brain tumors, a preliminary report. 858 40

Vascular endothelial growth factor (VEGF) is an angiogenic factor which is known to be expressed in several malignancies including glioma. The effect of transforming growth factor-beta (TGF-beta) isoforms as well as gangliosides on VEGF production was investigated in human glioma cell lines. TGF-beta isoforms and gangliosides were found to differentially stimulate VEGF production by these cells. The ganglioside GD3 enhanced this release to the greatest extent and the stimulation was more marked in a glioblastoma cell line than in the two other anaplastic astrocytoma cell lines. These results suggest that both TGF-betas and gangliosides may act as indirect angiogenic factors by stimulating VEGF secretion.
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PMID:Vascular endothelial growth factor production is stimulated by gangliosides and TGF-beta isoforms in human glioma cells in vitro. 860 72


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