Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metastatic brain tumors very often cause severe brain edema. We examined ultrastructural findings of capillaries of these tumors and discussed the causes of cerebral edema as compared with those of glioblastoma which were previously reported. Four specimens were examined: two adenocarcinomas from the lung, one squamous cell carcinoma from the lung and one adenocarcinoma from the breast. These replicas and ultrathin sections were examined by transmission electron microscope. The following characteristic structures were detected; the capillary endothelium was proliferated, had marked infolding, and an increased number of pinocytotic vesicles and vacuoles. Short and elongate intercellular junctions were present. No open junction was detected. The basal lamina lost its three layered appearance and was irregular in width. Among these, an appearance of capillary fenestration was the most conspicuous features and observed in almost all capillaries. Two different pathogenesis for making vasogenic edema are proposed in metastatic brain tumor and glioblastoma. The frequent fenestration of the former and activated pinocytotic vesicles of the latter are responsible for extravasation of the edema fluid. The differences in distribution patterns of fenestration in metastatic brain tumor cannot be identified with respect to histological types.
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PMID:[Ultrastructure of capillary permeability in human brain tumor--Part 6: Metastatic brain tumor with brain edema]. 339 12

The effects of heat and antitumor drugs on malignant brain tumor cell lines were studied. A human glioblastoma cell line (SKMG1) and rat malignant brain tumor cell lines (T9, EB 679 and TR 481) were used in this experiment. Five different modalities of treatment with heat and drugs were used as follows: (Group 1) exposure to heat alone at 42 degrees C for one hour; (Group 2) exposure to antitumor drug alone for one hour (ACNU 2.5 or 5 micrograms/ml, ACR 0.02 micrograms/ml and CDDP 1 microgram/ml); (Group 3) simultaneous exposure to heat at 42 degrees C and drug for one hour; (Group 4) heat at 42 degrees C given first for one hour, followed by one hour exposure to drug one hour later ("preheating"); (Group 5) drug given first for one hour, followed by one hour exposure to heat at 42 degrees C one hour later ("postheating"). After each treatment, the inhibition rate at 4 days was evaluated and compared for each group. A synergistic effect was observed in Group 3. For example, when T9 cells were exposed to ACNU and to heat at 42 degrees C at the same time for one hour, inhibition rate was 78%, while the rates for Group 1 and Group 2 were 7% and 21%, respectively. The cytotoxicity of simultaneous treatment with antitumor drugs (ACNU, ACR and CDDP) and hyperthermia at 42 degrees C was apparently superior to that of other treatment modalities.
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PMID:[The effect of hyperthermia and antitumor drugs on brain tumor cell lines]. 346 29

The biodistribution, blood clearance, and in vivo transformation of cisplatin (cisdiaminedichloroplatinum, DDP) were studied in rats using 13N-labeled and unlabeled DDP. Following the i.v. injection of [13N]DDP, virtually no 13N activity was detected in brain tissue, and no measurable amount of the 13N label was displaced from [13N]DDP. Based on these results, [13N]DDP/positron emission tomographic (PET) scans were performed in two glioblastoma patients undergoing Phase II intra-arterial (i.a.) DDP chemotherapy: [13N]DDP was infused i.v. over 13-15 min, during which time serial PET scans were obtained. One hour later, [13N]DDP mixed with cold DDP (100 mg/m2 therapeutic dose) was infused at the same rate i.a., and a second sequence of PET scans was acquired. The pharmacologic advantage of i.a. administration was calculated as the ratio of integrated tumor/brain count ratios for the i.a. and i.v. studies. Our preliminary results demonstrate the feasibility of quantifying the pharmacologic advantage of i.a. DDP chemotherapy in individual brain tumor patients using [13N]DDP and PET.
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PMID:[13N]cisplatin PET to assess pharmacokinetics of intra-arterial versus intravenous chemotherapy for malignant brain tumors. 350 Feb 86

16 different free amino acids were determined in cerebrospinal fluid and plasma of each 5 patients with glioblastomas, meningiomas, and low grade gliomas as well as in 21 patients with lumbar disk herniations (control group). The values from the control group were in good accordance with those previously observed in normal adults of 5 studies of the literature. Significant changes were seen only in 6 of 16 amino acids. Absolute values of free CSF amino acids showed significant lower levels of valine, leucine and asparagine in the 3 subgroups whereas serine remained constantly high. The greatest changes were observed in glioblastoma and meningioma patients. Relative values gave similar results. No significant changes were found in CSF-plasma free amino acid relations. The authors conclude that changes of free CSF amino acids are due to a non-specific reaction of the brain itself to tumor growth. The different histology of the tumor does not give specific results. Determination of free CSF amino acids may help in early diagnosis of brain tumor recurrence after operation and to watch the effect of chemotherapy and radiation on brain tumor growth.
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PMID:[Cerebrospinal fluid and plasma aminograms in patients with primary and secondary tumors of the CNS]. 361 Mar 11

8 cases were studied to determine whether immunohistochemical investigation with anti-GFAP could contribute to confirming a primary brain tumor origin for an extracranial metastasis. The materials studied consisted of 3 glioblastomas, 3 anaplastic astrocytomas, and 2 medulloblastomas, along with their extracranial metastases. GFAP could be immunohistochemically demonstrated in all 6 primary glial tumors as well as in the metastases of the 3 astrocytomas and of 2 glioblastomas. The medulloblastomas and their metastases were immunohistochemically GFAP-negative. GFAP is thus a marker for extracranial metastases of astrocytomas and glioblastomas. A negative result however does not exclude the possibility that a metastasis is of glial origin as shown by the GFAP-negative metastasis of the one glioblastoma.
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PMID:[Significance of immunohistochemistry in neuro-oncology. I. Demonstration of glial fibrillary acid protein (GFAP) in extracranial metastases from primary brain tumors]. 391 31

The histological classification, pathophysiology, and treatment modalities of malignant gliomas (glioblastoma, malignant astrocytoma) were reviewed with reference to the WHO classification of primary brain tumors and the recent progress made in glioma biology. Patients with glioblastoma and malignant astrocytoma showed, respectively, 10.6% and 22.2 of the five-year survival rate according to the All Japan Brain Tumor Registry. In order to improve the prognosis of malignant glioma patients, many clinical trials have been conducted throughout the world. Malignant gliomas that grow in and invade the brain parenchyma cannot be cured by surgical resection. One should treat the residual tumor with irradiation, chemotherapy and immunotherapy. Radiation therapy alone and radiation therapy plus chemotherapy using nitrosoureas or procarbazine have been proved statistically to be more effective for malignant gliomas than supportive care and radiation therapy alone, respectively. Prospective clinical trials support the view that malignant gliomas should be treated vigorously using a multimodal approach that includes surgical resection, high-dose radiation therapy, and prolonged maintenance chemotherapy.
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PMID:[Treatment modalities for malignant gliomas with reference to their pathophysiology]. 394 92

Ten patients with malignant brain tumor (8 cases with glioblastoma, 2 cases with medulloblastoma) were treated with a new water-soluble nitrosourea, MCNU. Objective tumor regression of tumor (CR & PR) on computerized tomography was observed in four patients (2 complete and 2 partial) after MCNU, chemotherapy showing a response rate of 40%. The major side effects of MCNU were mild or moderate myelosuppression, and some cases also showed gastrointestinal toxicities and impairment of hepatic function. However, all these side effects were mild and transient and soon recovered to normal levels. One patient with glioblastoma multiforme recurrence was treated with a high-dose chemotherapy of MCNU (400 mg) associated with autologous bone marrow transplantation. Myelosuppression began to appear from 15th day of MCNU administration and normalized within 30 days afterwards. These results suggest that MCNU therapy is effective for patients with malignant brain tumors.
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PMID:[Effect of MCNU on brain tumors. Part II: Clinical experience with MCNU on malignant brain tumors]. 609 64

This is a paper of new trial of treatment of malignant brain tumor by local injection of bleomycin (BLM). The new method of intraneoplastic BLM injection is as follows: in the cases ended up with subtotal or partial removal of the tumor, Ommaya's device was detained in the tumor bed, and its reservoir was fixed subcutaneous on the skull. 0.1 mg/kg to 0.2 mg/kg of BLM was injected by subcutaneous puncture into the reservoir every other day. Usual total dose of BLM was 30-80 mg. The patients were usually treated with 60Co-irradiation and immunotherapy after local injection of BLM. Twelve patients with malignant brain tumor were treated by the above mentioned new method and a follow-up study was done. One-year survival rate was 50% and three-year survival rate was 25%. Each case of primary sarcoma, medulloblastoma and malignant oligodendroglioma survived for a very long time. However, most of the patients especially those with glioblastoma died of recurrence in about one year or so inspite of temporary improvement of their clinical symptoms and clinical findings. In the autopsy cases of malignant gliomas, similar pathological findings were obtained around the tumor bed. In macroscopical view, the extensive necrotic foci and small haemorrhages were observed around the tumor bed not deeper than 2 to 3 cm from the surface of the cavity, and in the deeper part the tumor tissues were actively proliferating. Microscopically there was a severe coagulation necrosis of tumor cells with haemorrhage, collagenous tissue proliferation, fibrin deposit, increasing capillary vessels and infiltrating lymphocytes and granulocytes. Consequently, the scintillation scanning of BLM labelled 57Co was utilized to make clearance curves of the drugs in the patients with malignant brain tumor. The results were as follows: 57Co-BLM activity in the tumor tissue decreased about 70% 2-4 days after local injection of the drugs, whereas, it decreased about 70% 2-4 hours after intravenous injection of the drugs. From these results it could be presumed that locally injected BLM remained in the tumor tissues for a longer time and killed malignant tumor cells completely. However, an unfavorable fact was that locally injected BLM was retained only within the tumor tissue less than 2-3 cm apart from the cavity, showing no efficacy enough to prevent tumor proliferation in more remote area. In conclusion, the local injection of BLM seems to be very effective for the treatment of malignant brain tumors if it is used together with intravenous or intraarterial injection of other chemotherapeutic drugs.
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PMID:[A new treatment of malignant brain tumor -1: local injection of bleomycin (author's transl)]. 617 6

Neocarzinostatin as previously reported, appeared to exhibit an intense cytotoxicity to the glioblastoma cells and some other malignant brain tumor cells, such as pineal germinoma or medulloblastoma, which are notoriously known to disseminate into the cerebrospinal fluid space. In vitro study, the minimum susceptibility of glioblastoma cells to neocarzinostatin was found to be below 0.005 microgram/ml, whereas normal glia cells were not affected at 0.3 microgram/ml. This study indicated that neocarzinostatin was extremely effective in the treatment of malignant brain tumor without affecting normal neural tissue. Pharmacokinetic study was performed in order to establish intermittent intrathecal perfusion therapy and to prevent subarachnoid dissemination of the brain tumor cells. Experimental results were applied to the treatment of 12 patients with brain tumor, who had shown positive cytology of the cerebrospinal fluid. Follow-up investigation showed quite a favorable result and it was considered that prophylactic irradiation to the entire spinal column could be replaced with intrathecal administration of neocarzinostatin. During clinical application no noticeable side effect was encountered and active stimulation of macrophages, which were mobilized into the CSF space, was another unexpected advantage of this treatment.
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PMID:[Pharmacokinetic one-compartment model using neocarzinostain as a prototype drug and its clinical application to chemotherapy for brain tumor. Part II. A clinical trial with selected protocol]. 622 89

A pharmacokinetic one-compartment model for the cerebrospinal infusion for the brain tumor chemotherapy is described together with various parameters used for computer simulation. An antitumor protein, neocarzinostatin (NCS) as a prototype drug, has been utilized since it was found effective against glioblastoma cells at extremely low concentration (less than 5 ng/ml) and it is readily inactivated by serum. A very slow infusion velocity was found necessary for an appropriate dose regimen; for example, 0.25mg of the drug should be infused into CSF for about 40 min to attain a drug level of 8 ng/ml.
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PMID:[Part I. Theory and computer simulation for cerebrospinal infusion]. 622 92


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