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)

Fifteen patients were treated in a Phase I study of intracarotid carboplatin (200-400 mg/m2) in 5% dextrose and water infused over 15 to 30 minutes through a transfemoral catheter with a 0.2-micron inline filter. This study was done because intravenous carboplatin has less neurotoxicity than cisplatin and is active against brain tumors. Eleven men and four women ranging in age from 37 to 72 years (median, 59 years) were treated. The Eastern Cooperative Oncology Group performance status was 1 in 3, 2 in 4, and 3-4 in 8 patients. Eight patients had one to three previous chemotherapy regimens; previous radiotherapy had failed in 13 patients. The response of patients in the Phase I study follows: glioblastoma, 6 failed; not evaluated because of early death from pulmonary embolus, 1; recurrent Grade II and III glioma, 1 stable (minor response with neurologic improvement) and 2 failed; malignant oligodendroglioma, 1 failed; brain metastases from nonsmall cell lung cancer, 1 partial remission, 1 stable (minor response), and 1 failed; brain metastases from unknown primary, 1 stable (minor response with neurological improvement). Median survival was 9 weeks. Nausea was mild to moderate. One patient had granulocytopenia, and 2 had thrombocytopenia (mild). At 200 mg/m2 (2 patients), 1 had a focal seizure. At 300 mg/m2 (9 patients), 2 with abnormally small arteries had severe pain early in the treatment and posttreatment ipsilateral conjunctival edema, decreased vision, and cerebral edema (with partially reversible increased hemiparesis); 1 other had mild decrease in ipsilateral vision and 1 had transient aphasia on removal of the catheter (possibly the result of a vascular spasm).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phase I study of intracarotid administration of carboplatin. 131 64

Among new therapeutic modalities for both primary and secondary brain tumors, selective manipulation of metabolic pathways seems attractive. In human malignant gliomas and cell lines from a glioblastoma multiform, lonidamine has been shown to interfere with aerobic glycolysis with a decrease of lactate production by the inhibition of a mitochondrially-bound hexokinase; this selective reduction of the energetic capabilities of glioma cells would be a limiting factor for processes requiring energy, such as cell growth and recovery from potentially lethal damage after radiotherapy or chemotherapy. The activity of lonidamine in malignant gliomas after surgery in association with conventional radiotherapy is being investigated, while previous studies have suggested a limited, but clear therapeutic activity of the drug in recurrent malignant gliomas. In brain metastases lonidamine has not been effective as a radiation enhancer, but has been shown to potentiate systemic chemotherapy. Most common side effects were myalgias, testicular pain and ototoxicity with no serious organ toxicity or myelosuppression.
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PMID:Lonidamine in malignant brain tumors. 203 Nov 97

In this study we tested the effect of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha) and a combination of these immunotherapeutics on clonogenic growth of cell lines and primary cultures of malignant human brain tumors. Out of 29 primary cultures studied, 5 were inhibited 50% or more by IFN-gamma (10 ng/ml), 6 were inhibited 50% or more by TNF-alpha (10 ng/ml) and 14 were inhibited 50% or more by a combination of IFN-gamma (10 ng/ml) and TNF-alpha (10 ng/ml). The doses of the immunotherapeutics used in this in vitro study are achievable in serum after intravenous administration of IFN-gamma and TNF-alpha without causing unacceptable side effects. We believe that some glioma patients and some patients with brain metastases will benefit from receiving treatment with IFN-gamma, TNF-alpha or a combination of these immunotherapeutics. The patients should be selected for treatment with these immunotherapeutics according to in vitro sensitivity results.
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PMID:Effects of interferon-gamma and tumor necrosis factor-alpha on clonogenic growth of cell lines and primary cultures from human gliomas and brain metastases. 250 Jan 40

Routinely processed biopsy material, including 56 gliomas of varying malignancy, 10 meningiomas, 10 brain metastases and 12 brain abscesses, was examined for the presence and distribution of IgG, IgA, IgM, IgD and albumin using the unlabeled antibody peroxidase-antiperoxidase technique. In all specimens the deposition of stained immunoglobulins (Ig) was strictly associated with that of albumin even on cell surfaces. Thus there was no evidence for specific membrane binding or cytotoxicity. The interstitial proteins demonstrated are most likely derived from the plasma by blood-brain barrier breakdown which occurs in nearly all tumors and abscesses. Obvious intracellular staining for Ig and albumin was seen in glioma cells and astrocytes only. This is suggested to be due to active protein uptake as a specific feature of astrocyte differentiation which decreases with malignancy and is lost in glioblastomas. Evidence for local Ig production was found in 8 out of 10 metastases with striking IgG- and IgA-positive plasma cells within lymphocytic infiltrations and in one meningioma showing conspicuous plasma cells components. No glioma contained Ig-bearing plasma cells, though round cell infiltrations were present in 64% of the unselected cases. The significance of these findings regarding the immunological situation in brain tumors is briefly discussed.
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PMID:Immunohistochemical demonstration of immunoglobulins and albumin in human brain tumors. 254 57

The proliferation rate of 40 intracranial neoplasms (30 gliomas, 1 hemangioblastoma, 3 meningiomas, 1 neurinoma and 5 brain metastases) was investigated using the monoclonal antibody Ki-67. In eleven of the gliomas recurrences could be observed, and two of them recurred for second time. In total the Ki-67 labelling indices of 53 specimens were investigated. The Ki-67 nuclear antigen was demonstrated in frozen sections by application of the appropriate monoclonal antibodies according to a modified alkaline phosphatase-antialkaline phosphatase (APAAP) technique. The proliferation rate was evaluated by cell count calculation of the staining index. Ki-67-labelled glioma cells varied from 0.2 percent in one meningioma (WHO-grade I) to 9.1 percent in one glioblastoma. In ten glioma recurrences, higher Ki-67 staining indices could be observed than in their primaries, even when the histological grading did not change substantially. In a cerebellar hemangioblastoma, a trigeminal neurinoma and two endotheliomatous meningiomas the fraction of stained nuclei was less than one percent; however, one recurrent transitional meningioma without any histological sign of malignancy showed a staining index of 2.4 percent. The staining indices of five brain metastases of different malignancies ranged from 1.5 percent in a malignant melanoma to 6.1 percent in bronchial carcinoma. In the majority of the cases examined, the percentage of Ki-67 labelled cells was in accordance with the histologic grade of the neoplasm. In general, there was a direct relationship between the number of stained nuclei and the frequency of mitoses (mitotic index) evaluated in hematoxylin-eosin stained frozen sections. Interestingly, the frequency of mitosis and stained nuclei were higher in tumor recurrences than in the primaries. The results of this study imply that immunohistological labelling of the proliferating cell fraction should become an important additional criterion to predict the biological behaviour of human nervous system neoplasms.
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PMID:Relationship between Ki-67 positive cells, growth rate and histological type of human intracranial tumors. 305 45

It is well known that convulsion is one of serious adverse reactions of x-ray contrast media. The occurrence of the convulsion seems to be very rare in general population. However, a few reports noticed recently that patients with brain metastases or gliomas developed this complication relatively frequently and the terms, as contrast-induced convulsion or contrast media-associated (induced) seizure, were used. We performed 12,479 cranial CT examinations with contrast enhancement during the last nine years. The amount of 100 ml in adult or 2 ml/kg in children of 65% Angiografin (methylglucamine diatrizoate) was given intravenously and five patients had contrast media-associated seizures. Case 1: A 37-year-old man with right frontal anaplastic glioma was treated surgically and with radiochemotherapy and hyperthermia. In spite of anticonvulsant therapy, general or left hemiconvulsions occurred sometimes. The patient had contrast-induced general convulsion at 16th CT examination which revealed enhancement in the wall of surgical tissue defect. At 26th CT study, he developed general convulsion again. Case 2: A 47-year-old man with anterior callosal anaplastic glioma was treated surgically and with radiochemotherapy and hyperthermia. After then, he had contrast media-associated general convulsion at 10th CT examination which showed enhanced lesions. Case 3: A 63-year-old woman had been treated surgically for lung cancer. Five years later, CT revealed a ring enhancement in the left frontal lobe. Radiation reduced the lesion gradually.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical course and CT findings in patients with contrast media-associated seizures]. 359 1

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

Six patients with multifocal glioma are presented. Computerized tomography revealed multiple, discrete, contrast-enhancing lesions in the cerebral hemispheres, suggestive of multiple intracranial metastases. The most accessible lesion was resected at craniotomy in each patient, confirming the diagnosis of primary malignant glioma. Postoperative radiation therapy and chemotherapy were instituted according to current protocols. Since neuroradiological studies may not allow distinction of multifocal glioma from multiple brain metastases, surgical biopsy is suggested in those patients who have no history of cancer.
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PMID:Computerized tomography findings in multifocal glioma. 628 Apr 51

A case of undifferentiated pancreatic carcinoma is described. The first symptoms were due to brain metastases and was then diagnosed as malignant glioma. The appearance of a sudden obstructive jaundice and pneumoperitoneum without any apparent cause led to the diagnosis of undifferentiated pancreatic carcinoma and peritoneal carcinomatosis, that was confirmed by the anatomicopathological study.
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PMID:[Cerebral metastasis, idiopathic pneumoperitoneum and obstructive jaundice as clinical manifestations of carcinoma of the pancreas]. 657 80

Although human glioblastomas are highly invasive tumors intracerebrally, only rarely do they metastasize outside the central nervous system. In contrast, the brain is a major target for metastatic spread of many systemic tumors. Recently, it was demonstrated that expression of splice variants of CD44 (CD44v), but not standard CD44 (CD44s), was sufficient to confer metastatic potential to low- or nonmetastatic rat tumor cells. Because CD44 is expressed in brain tumors, we examined whether differential expression of CD44 isoforms was correlated with the metastatic behavior of these tumors. We compared CD44s and CD44v expression in 17 human glioblastomas, 18 glioma cell lines, and metastases of 15 other tumors to the brain by reverse transcription/polymerase chain reaction, Northern blotting, and immunocytochemistry. These experiments showed that 0 of 17 glioblastomas and 0 of 18 glioma cell lines expressed CD44v as compared to 12 of 15 brain metastases. These data show a correlation between CD44v expression and the metastatic ability of the tumors analyzed (P < 0.01). This suggests (a) that the biological significance of the lack of CD44v expression in human glioblastomas warrants further examination with regard to their inability to metastasize extraneurally and (b) that CD44v expression may play a role in the intracerebral spread of about 80% [corrected] of the brain metastases. Therefore, CD44v expression should be further considered as a potential marker for differential diagnosis and prognosis of patients with brain metastases.
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PMID:Variant CD44 adhesion molecules are expressed in human brain metastases but not in glioblastomas. 769 37


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