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

The rational application of chemotherapy in tumors of the central nervous system is discussed in particular the use of the new derivatives of nitrosourea: BCNU (1-3 bis-(2-cloroetil) 1-nitrosourea) and CCNU (cloroetil-cicloesil-nitrosourea). The results of therapy with antimetabolites, alkylating agents, antibiotics, and plant alcaloids, are reported as well as those obtained with radio - sensitizing substances (containing B10 or BUdR, IUdR, FUdR). The results obtained in the United States and in Japan with BCNU and CCNU are considered as well as the personal data of 43 cases treated with BCNU and 10 cases treated with CCNU (including intracranial glial tumors, spinal glial tumors and metastatic tumors of the central nervous system).
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PMID:[The chemotherapy of tumors of the central nervous system (author's transl)]. 18 61

A patient with a mixed malignant glioma metastatic to the bones and lungs failed to respond to two different broad-spectrum combination chemotherapy regimens which included Adriamycin, methotrexate, cyclophosphamide, CCNU and cis-dichlorodiammineplatinum(II).
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PMID:Combination chemotherapy for extracranial metastases of a primary malignant cerebral neoplasm. 47 15

Intracerebral murine glioma 26 was used as a model system for evaluating two-drug combinations of antitumor agents, BCNU was combined with either procarbazine, dianhydrogalactitol, or ellipticine. CCNU was combined with procarbazine. All combinations were more active than the individual drugs alone. The most potent combinations achieved 85-100% tumor "cure" at 120 days, with combined toxicity indices of 0.25 (CCNU-procarbazine) to 1.30 (NCNU-dianhydrogalactitol). The experimental data were compared to clinical studies with CCNU, procarbazine, and vincristine, and BCNU-procarbazine.
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PMID:Correlations between experimental chemotherapy in the murine glioma and effectiveness of clinical therapy regimens. 75 Jan 3

The effects of antineoplastic treatment on gliomas are related to tumour cell cycle and proliferation kinetics, glioma tissue architecture, and the surrounding environment. Morphological changes induced by radiation and chemotherapy are characterized by cell necrosis and severe alterations in cell and nuclear morphology caused by changes in the cell kinetic parameters which, however, may also occur spontaneously in untreated anaplastic gliomas. Comparative studies of cytological imprints and routine histological preparations of biopsy and autopsy specimens were performed in four groups of anaplastic astrocytomas and glioblastomas (78 cases) with postsurgical irradiation, combination chemotherapy, and CCNU treatment, and without specific postsurgical treatment (control group). Following radiation and chemotherapy, in addition to increased necrosis and vascular response, a variety of characteristic but nonspecific changes were observed in cell and nuclear morphology with prominent formation of multinucleated giant and monstrous cells, irregular and hyperchromatic nuclei, and severe cytoplasmic degeneration indicating both inhibition of cell division and cell damage. Statistically significant findings were a posttreatment increase in the number of multinucleated giant and monstrous cells and a decrease in the number of mitoses. These changes were more pronounced after chemotherapy than after radiation, while no significant dissimilarities were found between combination chemotherapy and CCNU. The implications of these changes on the mechanisms of antitumour treatment in anaplastic gliomas are discussed.
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PMID:Morphological changes in anaplastic gliomas treated with radiation and chemotherapy. 83 84

We attempted to show a dose effect relationship for radiation therapy by treating patients harbouring malignant glioma with increasing doses of radiation in a step-wise fashion. We postulated that no increase in delayed toxicity would be seen because we used hyperfractionation technique. Between January 1981 and December 1988 we treated 280 patients three times daily at 4 hour intervals. 100 patients received a total dose of 6141 cGy, 73 patients received 7120 cGy, and 107 patients received 8000 cGy. CCNU was given at the time of tumor progression following radiotherapy. Median time to tumor progression was 28 weeks for patients who received 6141 cGy, 27 weeks for patients who received 7120 cGy and 36 weeks for patients who received 8000 cGy. Median survival was 46 weeks for patients who received 6141 cGy, 38 weeks for patients who received 7120 cGy and 45 weeks for patients who received 8000 cGy. There was no statistically significant difference in either time to tumor progression or survival among the three treatment arms and no dose response effect was seen. There was no increase in delayed radiation toxicity when the total radiation dose was increased up to 8000 cGy.
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PMID:Increasing radiation dose intensity using hyperfractionation in patients with malignant glioma. Final report of a prospective phase I-II dose response study. 133 44

In the period from Jan 1 1984 to Dec 31 1990 clinical and radiological evidence of brain glioma was found in 120 cases treated previously surgically. The group comprised 55 women (46%) and 65 men (54%). At the time of tumour diagnosis their age was ranged 40 to 60 years. All patients received non-radical surgical treatment, supplemented with Co60 radiation in 104 cases, in 3 cases Co60 treatment was given together with chemotherapy (CCNU) and 12 patients received no complementary treatment. Thirty four patients (28%) had reoperations, in two cases even twice. In 86 cases (72%) treatment was palliative. Three types of secondary tumour regrowth were discerned. Reoperation prolonged survival and its effectiveness was greatest in regrowth type I. The shortest survival till the appearance of regrowth signs and the shortest survival after recurrence were in type II of regrowth.
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PMID:[Diagnosis and treatment of recurrent brain glioma]. 140 84

Aggressive oligodendrogliomas, tumors that are symptomatic, enlarging, enhancing, and usually but not always anaplastic, respond to chemotherapy. We have observed responses to chemotherapy in 18 of 19 consecutively treated patients with newly diagnosed or recurrent aggressive oligodendrogliomas. A regimen of procarbazine, CCNU (lomustine), and vincristine (PCV) is predictably effective, but other drugs have antioligodendroglioma activity. Cooperative group trials will be necessary to determine the most effective drug, or combination of drugs, and to explore fully the role of chemotherapy in the treatment of this uncommon glioma.
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PMID:Aggressive oligodendroglioma: a chemosensitive tumor. 164 Nov 13

A cell line, 497-P(1), derived from the VM spontaneous murine astrocytoma has been used to develop an in vitro therapeutic model of human glioma. In this study we describe the preparation of MTS from this cell line. The in vitro chemosensitivity of 497-P(1) MTS has been examined and compared to the sensitivity of the monolayer culture. BCNU and CCNU both produced growth delay in MTS at doses below the ID50 of the monolayer culture. MTS, however, were considerably more resistant to vincristine and procarbazine when compared to the monolayer culture.
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PMID:The VM model of glioma: preparation of multicellular tumour spheroids (MTS) and their response to chemotherapy. 226 97

Using a cell line derived from the VM spontaneous murine astrocytoma, a reliable in vitro-in vivo model of human malignant glioma has been developed. In this paper we examine the effects of cytotoxic drugs with known activity against other animal brain tumour models and human disease on the in vivo VM model. The drugs BCNU, CCNU and vincristine produced significant volume reduction in tumours growing at a subcutaneous location in syngeneic animals. Procarbazine was ineffective. Similarly, BCNU, CCNU and vincristine produced small but statistically significant increases in survival of VM mice bearing the intracerebral tumour, but procarbazine was again ineffective. The modest, but significant, response of the VM model to the nitrosoureas mimics the human situation more closely than previously described animal models.
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PMID:The chemotherapeutic response of a murine (VM) model of human glioma. 229 89


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