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)

Sixty-five patients with malignant brain tumors were treated with a combination of BCNU (100 mg/m2 qd X 1) and procarbazine (100 mg/m2 qd X 14); the cycle was repeated in 1 month and then on a 6-week schedule with procarbazine being given for 21 days. Forty-five patients had malignant gliomas (glioblastoma multiforme, anaplastic astrocytoma, malignant glioma, or gemistocytic astrocytoma) and were evaluated as a group. All patients had either shown evidence of tumor regrowth after previous surgery and/or radiotherapy, or had deep unbiopsied tumors presumed to be malignant gliomas. Of these 45 patients, 13 of 45 (30%) were judged to be unequivocal responders and an additional eight of 45 (17%) were designated as probable responders. The median duration of clinical response was 34 weeks for responders and 20 weeks for probable responders. The combination of BCNU and procarbazine, therefore, was somewhat inferior to a previous combination of procarbazine, CCNU, and vincristine.
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PMID:BCNU (NSC-409962) and procarbazine (NSC-77213) treatment for malignant brain tumors. 17 10

Histopathological examinations were made on tumors of the nervous system induced in rats of Donryu strain by weekly intravenous injections with N-nitroso-methyl-urea (NMU) or by a single administration of NMU through the mothers. A total of 176 neural and nonneural neoplasms were produced in this study. It was suggested that the fetal nervous system of Donryu rats was also highly susceptible to the oncogenic effects of NMU. Of these tumors produced, those of the peripheral nervous system amounted to 121, comprising 68.7% of the total number of the neoplasm. Microscopically, most of the nerve tumors showed the histology corresponding to that of human neurinomas. Many tumors, however, disclosed more or less anaplastic cytological appearance. Fifteen gliomas were produced in the brain and spinal cord. Microscopically, they were classified into mixed glioma, oligondendroglioma and anaplastic astrocytoma. The commonest brain tumors produced in rats from intravenously treated group were periventricular mixed gliomas, while gliomas in rats from transplacentably treated group showed an isomorphic histology with a close resemblance to that of oligodendroglioma.
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PMID:Histopathological studies of the nervous system tumors in rats induced by N-nitroso-methyl-urea. 118 45

We reviewed 11 consecutive patients with an antemortem cytologic diagnosis of meningeal gliomatosis. In three patients, meningeal gliomatosis was diagnosed before surgical resection of the glioma. Three of five patients with anaplastic astrocytoma and one with oligodendroglioma improved with treatment. Patients with glioblastoma multiforme did not respond and had a median survival from the diagnosis of meningeal gliomatosis of only 8 weeks. Meningeal gliomatosis can be an early finding in gliomas. Treatment response is probably related to tumor histology and grade.
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PMID:Clinical outcome in aggressively treated meningeal gliomatosis. 131 Mar 53

The frequency of nucleolar organizer regions (NORs) in each glioma tissue and the relation between the expression of glial fibrillary acidic protein (GFAP) and the frequency of NORs was investigated. The number of Ag-NORs per cell for glioblastoma multiforme was significantly higher than that for anaplastic astrocytoma (P less than 0.05) and that for astrocytoma (P less than 0.01). The number of Ag-NORs per cell for GFAP-positive cells was significantly lower than that for GFAP-negative cells in each histopathological grade (P less than 0.01). Moreover, the linear relationship was demonstrated between the Ag-NORs numbers of GFAP-negative cells and bromodeoxyuridine (BUdR) labeling indices. From these results, it is concluded that many GFAP-positive glioma cells may have low growth potential in glioma tissue and GFAP-negative cells may have a close relation to cell proliferation. The combination of immunohistochemical and silver colloid staining is a useful method for investigating the biological characteristics of brain tumors.
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PMID:Glial fibrillary acidic protein (GFAP) expression and nucleolar organizer regions (NORs) in human gliomas. 131 73

In experiments to identify molecules that might be important in the pathogenesis of glioblastoma multiforme, the most common malignant brain tumor, we found that annexin II (Lipocortin 2, p36), a likely second messenger in several different mitogenic pathways, was highly expressed in tumor tissue of glioblastoma multiforme (9 of 9) and highly anaplastic astrocytoma (2 of 6), but not in astrocytomas of lower pathological grade (0 of 6). We also detected high levels of annexin II expression in fetal brain during the period when radial glia proliferate, although annexin II expression was not detected in normal adult brain. These data demonstrate that annexin II expression is developmentally regulated in the human central nervous system and suggest that the early progenitor radial glia share important characteristics with highly malignant glial tumors.
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PMID:Developmental regulation of annexin II (Lipocortin 2) in human brain and expression in high grade glioma. 133 84

Long-term survival after the diagnosis of malignant glioma is uncommon but not rare. To define better the population of patients who have extended survival with this disease, we reviewed the records of 22 of our patients who survived more than 4 years after the biopsy-proven diagnosis of anaplastic astrocytoma, malignant mixed glioma, or glioblastoma multiforme. Surprisingly, 21 of the 22 patients are still alive and being actively followed by the authors. The long-term survivors were typically young and with minimal or no functional impairment at the time of diagnosis. Survivals ranged from 4.2 to 15.8 years. The quality of survival was generally good, with the surviving patients having a mean Karnofsky Performance Score of 76. Three-quarters of the patients had no enhancement or mass effect on their most recent computed tomography scans. A review of the available literature, together with our own series, suggests that death from recurrent disease is unusual in glioma patients who survive more than 4 or 5 years.
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PMID:Long-term survival after the diagnosis of malignant glioma: a series of 22 patients surviving more than 4 years after diagnosis. 133 26

Congenital brain tumor is a rare disease in the neonatal period. According to the literatures, they comprise only about 1% of childhood brain tumors. Among the congenital brain tumors, 10%-25% are astrocytomas. Anaplastic astrocytoma is one of the malignant glioma. The prognosis is usually not good in the childhood or adult stage. We report one case of congenital anaplastic astrocytoma who received combination chemotherapy, including vinblastine, cisplatin and etoposide following subtotal resection of tumor. After chemotherapy, he got a favorable outcome. And now, he is still no evidence of tumor recurrence for two years.
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PMID:[Successful treatment of congenital anaplastic astrocytoma by combining vinblastine, cisplatin and etoposide: a case report]. 133 32

This study investigated the secretion of a tumor necrosis factor (TNF) and lymphotoxin (LT) from lymphokine-activated killer (LAK) cells during co-culture with glioblastoma cell lines, autologous glioma cells, and other non-gliomatous tumor cell lines (K562 and Daudi). Cytokine secretion from peripheral blood mononuclear cells (PBMC) was also examined. The TNF activity of culture supernatants was measured by L cell cytotoxic assay, and a neutralization test using anti-TNF and/or anti-LT antibodies determined whether the cytotoxic activity was due to TNF or LT. The results show that LAK cells secrete both TNF and LT during monoculture and release increased amounts of TNF and LT with non-gliomatous tumor cell stimulation, but PBMC secrete only TNF with tumor cell stimulation. Glioblastoma or anaplastic astrocytoma cells, however, did not stimulate cytokine secretion from either LAK cells or PBMC. This indicates a discrepancy between the capability of LAK cells to lyse malignant glioma cells and cytokine secretion from LAK cells, and suggests that malignant glioma cells may produce some factors which inhibit cytokine secretion from LAK cells.
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PMID:Analysis of tumor necrosis factor and lymphotoxin secreted by incubation of lymphokine-activated killer cells with tumor cells. 137 61

A case of cystic optic glioma involving chiasma and bilateral posterior optic pathway was reported. A 26-year-old male was admitted to our hospital complaining of dysarthria and left hemiparesis. CT, MRI revealed a cystic tumor at the right basal ganglia to midbrain, a calcified one at the bilateral optic tract and left temporal to thalamic region, and a small one at the chiasma. Radiotherapy and chemotherapy were performed because anaplastic astrocytoma was suspected after stereotactic biopsy of the tumor at the right basal ganglia. The subsequent MRI showed continuity among the above three lesions to be well defined. About 2 years later, however, enlargement of the cyst, tumor invasion beyond the optic pathway and growth of the chiasmal lesion were noted, and direct surgery to the chiasmal lesion was performed. The chiasma was swollen and grayish soft tumor tissue was partly resected after aspiration of the intrachiasmal cyst. The definitive pathological diagnosis was pilocytic astrocytoma. This case was designated as a peculiar optic glioma in the following respects; the patient was an adult man suffering from dysarthria and left hemiparesis, the tumor involved not only the chiasma and the bilateral optic tract, but also the outside optic pathway and was accompanied by a large cyst.
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PMID:[A case of cystic optic glioma involving chiasma and bilateral posterior optic pathway]. 144 96

Phase III Trial 8,301 tested the efficacy and safety of intraarterial (IA) BCNU for the treatment of newly resected malignant glioma, comparing IA BCNU vs intravenous (IV) BCNU (200 mg/m2 q 8 wks), each regimen without or with IV 5-FU (1 g/m2/d x 3 two wks after BCNU). All patients also received radiation therapy. 505 patients entered the study; 448 were in the Valid Study Group (VSG). Excluding 190 patients who for medical reasons were not eligible for IA BCNU, 315 patients were randomized between IA (167) and IV (148) BCNU. Actuarial analysis (log-rank) demonstrated worse survival for the IA group (p = 0.002). Serious toxicity was observed in the IA group; 16 patients (9.5%) developed irreversible encephalopathy with CT evidence of cerebral edema, and 26 patients developed visual loss ipsilateral to the infused carotid artery. 5-FU did not influence survival. Survival between the IV and the IA BCNU patients with glioblastoma multiforme did not differ, but was worse for IA BCNU patients with anaplastic astrocytoma than for IV BCNU (p = 0.002). Neuropathologically, IA BCNU produced white matter necrosis. IA BCNU is neither safe nor effective. Phase II Trial 8420, compared IA cisplatin, 60 mg/m2 every 4 wks, vs IV PCNU, 100 mg/m2 q 8 wks; 311 patients were randomized. Preliminary results have been presented. Severe encephalopathy occurred in only 1.5% of patients receiving IA cisplatin. The median survival of the IV PCNU patients was 11.8 months; that of the IA cisplatin patients was 9.4 months, not statistically different.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chemotherapy of malignant gliomas: studies of the BTCG. 144 62


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