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)

CCNU chemotherapy prolongs survival of patients with primary brain tumor when given at the time of tumor progression following radiation therapy. Used as single agent, response rates of 30 to 80 per cent have been reported with median response durations of five to six months. Experimentally, tumor cytotoxicity is enhanced using the combination of misonidazole and CCNU, without increasing myelotoxicity. In this phase I/II study, 23 patients with primary brain tumor which progressed following radiation therapy were treated with combined CCNU and misonidazole. In all patients either the diagnosis of high grade glioma was made at the time of initial diagnosis prior to radiation therapy or the tumor transformed from low grade to high grade glioma at the time of progression following radiation therapy. CCNU 120 mg/M2 was given four hours following misonidazole 3.5 g/M2 every six weeks, with dosage adjustments for myelotoxicity. Treatment was continued for one year or until tumor progression. Of the 17 patients in the study for one year or more, 11 (65 per cent) survived for one year, and six (35 per cent) remained free of tumor progression for one year. Median time to tumor progression from start of CCNU plus misonidazole chemotherapy was 27 weeks and median survival was 80 weeks. No severe complications resulted from myelotoxicity. One patient developed mild peripheral neuropathy which disappeared following discontinuation of misonidazole.
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PMID:Misonidazole and CCNU chemotherapy for recurrent primary brain tumor. 303 64

Data obtained during post-surgical monitoring (2 to 28 months) of 32 histologically confirmed malignant supratentorial glioma patients, are reported here. It was observed that: whatever the grade of malignancy, 100% of the patients whose tumor recurred showed, on at least one occasion, abnormal red blood cell (RBC) spermidine (SPD) (greater than 14 nmoles/8.10(9) RBC) or spermine (SPM) (less than 2 nmoles/8.10(9) RBC) levels. 30% of the patients whose tumor recurred had abnormal RBC polyamine concentrations, one to six months before any other sign of tumor progression. In patients with normal RBC polyamine values, clinical and tomodensitometric indications of tumor progression have to be reconsidered. During individual follow-up, RBC SPD levels of each patient were generally significantly correlated to those of SPM, and the slopes of their straight regression lines (SRL) appeared to be related to the importance of the intracranial cell proliferation. In such conditions we established the regression equation of the group of all recurring patients taken together. We propose a graphic model, including a space corresponding to RBC SPD and SPM levels observed in case of tumor recurrence, which can be utilized routinely in neuro-oncology during the monitoring of post-operative malignant supratentorial glioma patients.
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PMID:Red blood cell polyamines as biochemical markers of supratentorial malignant gliomas. 356 81

Intracarotid BCNU (100 mg/m2) and cisplatin (60 mg/m2) were administered to 36 patients with malignant brain tumors recurrent or progressive after cranial irradiation. Courses of therapy were repeated at 4-6 week intervals. Of 23 evaluable patients with recurrent glioma, 9 (39%) had tumor regression by CT scan and 3 had stable disease. The median time to tumor progression for responding patients was 37 weeks. For all patients with primary tumors it was 14 weeks. Six of 9 patients with no prior chemotherapy had a response and 1 had stable disease. Of 14 patients who had received prior chemotherapy, 3 had a response and 2 had stable disease. Survival ranged from 9 weeks to 95+ weeks (median 34 weeks) from start of therapy. Six of 23 patients with primary tumors are alive 1 year or more following therapy. Four of 11 patients with brain metastases had a response and 2 had stable disease. Major neurologic toxicity of intracarotid BCNU and cisplatin appeared cumulative and consisted of reversible hemiparesis in 3% of 118 courses, TIA in 1%, expressive aphasia in 9%, lethargy in 3%, seizures in 12%, and reversible confusion in 1%. Retinal toxicity consisted of mild blurring of vision in 4 patients and ipsilateral blindness in 5 patients. Three of 22 patients who had received supraophthalmic infusion later developed evidence of leukoencephalopathy. Intracarotid BCNU and cisplatin appears to have modest increase in activity over intracarotid cisplatin alone (Cancer 54:794, 1984), however, neurologic and retinal toxicity may also be increased.
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PMID:Phase II trial of intracarotid BCNU and cisplatin in primary malignant brain tumors. 370 37

Multiple daily fractionated radiation therapy (MDF) may be more effective than conventionally fractionated radiation therapy (CF) in the treatment of malignant glioma. The hypoxic cell sensitizer misonidazole (MISO) could be more effective when employed with small fractions of radiation every 4 hours to take advantage of the long half-life of the drug. To evaluate MDF and MDF in combination with MISO, a randomized prospective trial was initiated. Between January 1981, and December 1982, patients with histologically verified astrocytoma with anaplastic foci or glioblastoma multiforme were randomized to CF (5800 cGy, 30 fractions, 6 weeks), MDF (6141 cGy, 69 fractions, 4 1/2 weeks, at 89 cGy every 4 hours 3 times daily) and MDF in combination with MISO (1.25 gm/M2 three times weekly for the first 3 weeks). In January 1983, the CF arm was dropped and a high dose MDF arm added (7120 cGy, 80 fractions, 5 1/2 weeks, at 89 cGy per fraction every 4 hours 3 times daily). CCNU chemotherapy was given at the time of tumor progression. One hundred and twenty-eight patients were evaluated (38 CF, 42 MDF, 37 MDF plus MISO, and 11 high dose MDF). Median survival was 29 weeks for CF, 45 weeks for MDF and 50 weeks for MDF plus MISO. Survival was significantly improved for patients treated with MDF compared to patients treated with CF (p less than .002). The addition of MISO to MDF did not result in further improvement in survival. Acute toxicity was acceptable. No clinically apparent delayed toxicity was observed.
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PMID:Misonidazole combined with hyperfractionation in the management of malignant glioma. 609 Mar 67

Metastatic spread of an optic glioma through a ventriculoperitoneal shunt resulted in the accumulation of malignant ascites in a young boy. Chemotherapy with vincristine, CCNU, and prednisone resulted in regression of the ascites and no further tumor progression. Extracranial metastasis of such a slow growing tumor is a rare occurrence; however, in this case, the spread through the shunt further emphasizes the need for protective filters in the shunts.
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PMID:Metastasis of an optic glioma through a ventriculoperitoneal shunt. 686 Oct 97

Fifty-eight patients harboring recurrent malignant brain tumors were evaluated. CCNU (110 mg/m2) was administered on Day 1, procarbazine (60 mg/m2) was administered daily for 14 days beginning on Day 8, and vincristine (1.4 mg/m2) was administered on Days 8 and 29 of each 6-week cycle of therapy. Therapy was continued until tumor progression was documented. Before each course, a neurologic examination was performed and radionuclide and computerized tomographic scans were obtained. Response and progression were defined as improvement or deterioration, respectively, in at least two of the three tests. Of the 46 patients harboring recurrent malignant gliomas, 12 (26%) responded to therapy, 18 (39%) had tumor progression, and 16 (35%) had disease stability. Nineteen of the 46 patients were not previously treated with another form of chemotherapy: eight (42%) responded to therapy, eight (42%) had disease stability, and only three (16%) had early tumor progression. The median time to tumor progression was 26 weeks for patients responding to therapy or having disease stability. Approximately 30% of the patients were alive without evidence of tumor progression at 1 year. Evaluated by time to tumor progression and rate of tumor response or stabilization, this combination was similar to the BCNU-5-fluorouracil combination used for patients harboring recurrent malignant glioma.
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PMID:Modified procarbazine, CCNU, and vincristine (PCV 3) combination chemotherapy in the treatment of malignant brain tumors. 740 56

The p16INK4A/MTS1 (p16) and p15INK4B/MTS2 (p15) genes map to 9p21 where genetic alterations have been frequently reported in various human tumors. Using the polymerase chain reaction (PCR), we investigated the loss of these genes on primary glioma samples and cultured glioma cells. All or any of three exons of the p16 gene were homozygously delted in 11 (35.5%) of 31 glioblastomas, none of 9 anaplastic astrocytomas and 5 astrocytomas, and in all 6 human glioma cell lines. Exon 2 of the p15 gene was homozygously deleted in 4 (12.9%) of 31 glioblastomas, but not in lower grade gliomas. It was homozygously deleted in 5 (83.3%) of 6 glioma cell lines. In 12 short-term cultures of cells derived from primary glioma samples, 5 (41.7%) and 2 (16.7%) glioblastoma-derived cells had homozygous deletion of all or any of the three exons of the p16 gene and exon 2 of the p15 gene, respectively. The deletion pattern of these genes in cultured cells was completely consistent with that seen in the primary tumors. Furthermore, two long-term cultures retained both genes that were identical to those in the original tumor tissues. Our results indicate that loss of the p16 and p15 genes may be involved in tumor progression in human gliomas, especially in the development of glioblastoma, that this loss may give growth advantage to the cells in culture, and that it is not the result of culture artifacts.
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PMID:Homozygous deletions of p16INK4A/MTS1 and p15INK4B/MTS2 genes in glioma cells and primary glioma tissues. 749 69

The effectiveness of in vivo suppression of neovascularization and growth of malignant glial tumors by in situ administration of an antibody directed against basic fibroblast growth factor (bFGF), a strong mitogen for cells of mesodermal origin, was tested. One hundred fifty congenitally athymic nude rats (han rnu/rnu) were implanted intracerebrally with U-87MG tumor cells, known constitutive producers of bFGF. The animals were randomly assigned to six groups of 25 animals each. Animals were treated by in situ application of saline (Group F), control antibody (Group D), or polyclonal anti-bFGF antibody (Group B). In additional groups a putative effect on tumor growth caused by the treatment application device itself (between growth control Groups A and E), and the effect of heat-inactivated tumor cells (negative control Group C) were tested. After 3 weeks of treatment, tumor progression and degree of neovascularization were morphometrically recorded. In the untreated Groups A and E massive tumor growth was recorded, consisting of 19.9% +/- 0.4% and 27.1% +/- 0.5%, respectively, of the total brain cross-sectional area. In Group C, no tumor growth occurred. In control Groups D and F tumor progression consisted of 18.6% +/- 0.4% and 18.5% +/- 0.4%, respectively, of the total brain cross-sectional area; whereas in the anti-bFGF treated Group B, significantly smaller tumor masses measuring 7.2% +/- 0.1% were recorded. New blood vessels were located both peritumorally and intratumorally and defined as numerical density and area fraction (number/area and area/area). Significantly more new blood vessels were found in Groups A, D, E, and F, ranging from 41,380/mm2 +/- 464/mm2 to 53,442/mm2 +/- 150/mm2 peritumorally and 51,846/mm2 +/- 495/mm2 to 64,660/mm2 +/- 183/mm2 intratumorally than in the anti-bFGF treated Group B, which numbered 8220/mm2 +/- 225/mm2 peritumorally and 16,554/mm2 +/- 236/mm2 intratumorally. The authors conclude that treatment with anti-bFGF antibody is effective in inhibiting tumor-induced angiogenesis and correlated tumor progression. However, owing to the character of the experimental system used, one cannot exclude the possibility that application of the specific anti-bFGF antibody also counteracts device-induced neovascularization. The authors suggest that combined surgical excision and adjuvant immunotherapy of tumors such as glioblastoma and other malignant brain tumors that express bFGF might prevent tumor recurrence.
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PMID:In vivo inhibition of angiogenesis and growth of the human U-87 malignant glial tumor by treatment with an antibody against basic fibroblast growth factor. 753 64

Gangliogliomas are generally low grade neoplasms composed of mixtures of neoplastic glial and neuronal elements whose origin and exact nature are still controversial. We studied a series of 60 intracranial gangliogliomas looking for coexistent cortical architectural abnormalities (cortical dysplasia, microdysgenesis) and to determine if tumor behavior correlates with MIB1 (marker of cellular proliferation) labeling. The patients included 34 males and 26 females who ranged in age from 6 months to 55 years (mean 20 years). Thirty-eight tumors (63%) were located in the temporal lobe and 6 (10%) in the frontal lobe. Fifty-four patients (90%) presented with seizures (most with intractable epilepsy) and the duration of seizures ranged from 1 to 38 years (mean 14 years). In all cases, the predominant glioma component resembled a low grade fibrillary astrocytoma. In 14 tumors (23%), an oligodendroglial component was present. In one case, the glial component resembled an anaplastic astrocytoma. The tumors were characterized variously by perivascular chronic inflammation (N = 45, 75%), vascular proliferation (N = 36, 60%), granular bodies (N = 54, 90%), binucleated neurons (N = 36, 60%), calcification (N = 28, 47%), and cystic degeneration (N = 26, 43%). Meningeal involvement by tumor was observed in five (8%) cases. In 38 patients, sufficient tissue was resected to evaluate for the presence of concomitant cortical architectural abnormalities. Cortical architectural abnormalities were identified near to but clearly separate from the tumor in 19 (50%) patients. Only four patients including the anaplastic tumor died with tumor progression. MIB1 indices (positive tumor cells/1,000 tumor cells counted) in 54 cases ranged from 0 to 10.2 (mean 1.1 +/- 1.0).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cortical architectural abnormalities and MIB1 immunoreactivity in gangliogliomas: a study of 60 patients with intracranial tumors. 754 47

Sixty-four adult patients with malignant glioma entered into a Phase II study on the use of accelerated hyperfractionated radiation therapy. Histology included anaplastic astrocytoma (AA) in 15 patients and glioblastoma multiforme (GBM) in 49 patients. Treatment consisted of radiation therapy doses of 66 Gy in 44 fractions in 22 treatment days in 4.5 weeks, fractions of 1.5 Gy, b.i.d. 1,3-bis(2-chlorethyl)-1-nitrosourea (BCNU) 80 mg/m2 and hydroxyurea 800 mg/m2 were both given on treatment days 1, 6, 11, 16, and 21 during the irradiation course. Median survival time for all 64 patients is 61 weeks (range; 12-163 weeks) from the date of starting irradiation. Median time to tumor progression (MTP) for GBM patients is 31 weeks, and 1-year and 3-year progression-free survival (PFS) are 16% and 0%, respectively, while MTP for AA patients is not attained yet, and 1-year and 3-year PFS are 100% and 73%, respectively. On univariate analysis of prognostic factors for GBM patients, younger age, total or subtotal tumor removal, and frontal tumor location are associated with a better prognosis. A multivariate analysis confirmed the importance of the extent of surgery and tumor site and revealed the interfraction interval (4.5-5.0 hours vs 5.5-6.0 hours, p = .041) as an important prognostic factor. Acute and late toxicity is not increased. Longer follow-up and more patients are needed to evaluate tumor control and toxicity in AA patients.
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PMID:Accelerated hyperfractionated radiation therapy for malignant glioma. A phase II study. 757 67


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