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)

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

Although medulloblastoma is said to be capable of astrocytic differentiation, the development of an astrocytic neoplasm in association with a medulloblastoma is extremely rare. We report the light and electron microscopic features of a supratentorial glioblastoma that occurred 13 years after radiation therapy for a cerebellar medulloblastoma. The diverse ultrastructural features of the glioblastoma may reflect the multipotentiality of the cells in medulloblastoma. An alternate interpretation is that the glioblastoma represents a radiation-induced neoplasm after therapy for a medulloblastoma.
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PMID:Glioblastoma multiforme occurring 13 years after treatment of a medulloblastoma. 625 97

Tumor tissues of glioblastoma multiforme, astrocytoma and medulloblastoma, maintained up to 21--28 days by gelfoam organ culture technique, were examined by scanning electron microscopy (SEM). Glioblastoma multiform has irregular cell surface and many cytoplasmic folds. Astrocytoma has many fibrils. The fibrils have smooth surface and are coiling. Fibrils of piloid astrocytoma are smooth and cylindrical. The focal thickness of fibrils are associated with so-called Rosenthal fiber. Capillary of astrocytoma has irregular surface and marked tortuosity. Medulloblastoma is composed of non-fibrillated round tumor cells. The tumor cells touch each other with short cell processes. These findings seemed to correspond to the malignancy of original tumor. Comparative observation of medulloblastoma maintained by monolayer cell culture with one maintained by organ culture, using light microscopy and scanning electron microscopy, was done. And medulloblastoma in monolayer culture was proliferated to two types of cells. One is epitheloid cell with taper cell processes, and the other is stellate cell with fine processes. In most organ culture, feature of cells corresponded to those observed in original surgical material by light microscopy.
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PMID:[Scanning electron microscopy of human cultured gliomas (author's transl)]. 625 76

In 10,995 consecutive medicolegal autopsies, there were 19 deaths due to an unsuspected primary intracranial neoplasm. Nine (47.4%) of the tumors were in the astrocytoma-glioblastoma category. The remainder included four cases of oligodendroglioma and one case each of medulloblastoma, microglioma, meningioma, teratoma, colloid cyst and pituitary chromophobe adenoma. In six cases, death occurred following abrupt loss of consciousness, or else the patient was found dead. In five of these six cases, there were no known preceding symptoms. The remaining 13 patients exhibited the characteristic symptoms produced by intracranial neoplasms, including symptoms of increased intracranial pressure, epilepsy, and psychiatric manifestations. Only one patient presented with a focal neurologic deficit which resolved in 24 hours. A comparison of the duration and type of symptomatology exhibited by these patients with a hospital patient population in which death was caused by a previously diagnosed primary intracranial neoplasm and an autopsy was performed underscored 1) the shorter duration of acute symptomatology, 2) the nonlocalizing nature of the symptoms manifested, 3) the lack of progression or change in symptoms in those patients in whom epilepsy was the primary manifestation of their underlying disease, and 4) the lower incidence of focal neurologic deficits as the presenting symptoms in our series.
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PMID:Sudden, unexpected deaths due to primary intracranial neoplasms. 626 83

The antigenic relationships between human tumors of neuroectodermal origin and fetal brain were investigated by the production of hybridoma antibodies derived from a fusion of P3-NS1/1-Ag 4-1 (NS1) myeloma cells with splenocytes from a mouse multiply immunized with an homogenate of second-trimester human fetal brain tissue. Two monoclonal antibodies (MAs), 4D2cl 6 and 7H10cl 4, were studied in detail by cell surface radioimmunoassay (CS-RIA), quantitative absorption, indirect immunofluorescence, and peroxidase-anti-peroxidase (PAP) immunohistology. MA 4D2cl 6 binds to 5 of 14 glioblastoma (GBM) cell lines, 1 of 2 melanoma cell lines, 1 of 3 neuroblastoma cell lines, and 1 of 5 fetal fibroblast lines by CS-RIA and to 13 of 13 GBM, 1 neuroblastoma, and fetal brain, liver, spleen, and adult spleen unfixed frozen tissue by PAP analysis. MA 7H10cl 4 binds to 13 of 14 GBM, 1 of 3 neuroblastoma, and 1 medulloblastoma cell line(s) by CS-RIA analysis and to 13 of 13 GBM, 1 neuroblastoma, fetal brain, liver, spleen, thymus, and adult spleen by PAP analysis. Control non-central nervous system tumors and normal adult tissue, including brain, were unreactive with both MAs by CS-RIA, PAP, and absorption analysis. Tissue distribution and localization analyses established that MAs 4D2cl 6 and 7H10cl 4 recognize specificities of shared fetal-neuroectodermal-lymphoid distribution which are operationally specific within the adult central nervous system and which are not related to previously described oncofetal or onconeural antigens.
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PMID:Expression of human fetal brain antigens by human tumors of neuroectodermal origin as defined by monoclonal antibodies. 627 12

The effects of mitogenic lectins Phytohemagglutinin (PHA), and Concanavalin A (Con A) on the growth rate of cells derived from glial tumors (astrocytoma, ependymoma, glioblastoma, medulloblastoma, and C6 rat glioma), neural crest tumors (neuroblastoma and schwannoma), and meningiomas were studied. The cell lines were of human and animal origin. The specificity of lectin binding to mitogenic receptors was evaluated using complementary monosaccharides. In all glial- and some neural-crest tumor-derived cell lines, there was a lectin concentration-dependent and cell density-dependent, biphasic growth rate response with stimulation at low and inhibition at high lectin concentrations. This response did not depend on the type of glial tumor, species of origin, or passage level in vitro. Although, in meningioma-derived cell lines, lectins did not induce a growth rate response, they caused morphological changes ("whorling"). Lectin stimulation in glial tumor-derived cell lines resembles that occurring in peripheral blood lymphocytes. Lectin-induced mitogenesis may lay the groundwork for the establishment of a model of glial cell proliferation, and that permits the evaluation of cell surface effects, intracellular mechanisms, and epigenetic factors in studies of tumors, neural development, and neuroimmunology.
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PMID:Mitogenic lectin receptors of nervous system tumors. Study of gliomas, neural crest tumors, and meningiomas in vitro using phytohemagglutinin and concanavalin A. 628 95

The antigenic relationship between human tumors of neuroectodermal origin and fetal brain were further investigated by characterization of two hybridoma antibodies derived from a fusion of P3-NS1/1-Ag 4-1 (NSI) myeloma cells and splenocytes hyperimmunized to second trimester human fetal brain homogenate. Monoclonal antibodies (MAs) 1H8cl 2 and 1H8cl 3 were analyzed by cell surface radioimmunoassay (CS-RIA), quantitative absorption, indirect immunofluorescence, and peroxidase-antiperoxidase (PAP) immunohistology. MA 1H8cl 3 is the more broadly reactive, binding to 9/14 glioblastoma (GBM), 2/3 neuroblastoma, 1/2 melanoma, and 1 medulloblastoma cell line(s) by CS-RIA analysis, and to 12/15 GBM, fetal brain, spleen, and liver, and adult spleen by PAP analysis. MA 1H8cl 2 is more restricted, binding to 7/14 GBM, 2/3 neuroblastoma, 1 medulloblastoma, and 2/3 fetal skin fibroblast cell line(s) by CS-RIA, and to 9/15 GBM and fetal brain and spleen by PAP analysis. Control non-central nervous system tumors and normal adult tissue including brain, thymus, lymph node, liver, kidney, lung, skin, and pancreas, were unreactive with both 1H8cl 2 and 1H8cl 3 by CS-RIA, PAP, and absorption analysis. The data presented here establish the unique nature of the detected antigenic specificities as compared to previously described oncofetal and onconeural antigens, and define two immune reagents which are operationally specific for tumors of neuroectodermal origin within the adult central nervous system.
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PMID:Human fetal brain antigen expression common to tumors of neuroectodermal tissue origin. 628 96

In a series of 26 consecutive autopsy cases of intracranial tumors of neuroectodermal origin, tumor seeding on the ventricular surface and in the subarachnoid space was studied. Five cases of glioblastoma multiforme, six of malignant astrocytoma, six of medulloblastoma, one mixed glioblastoma-fibrosarcoma, one unclassified glioma, and one ependymoma showed ventricular and/or subarachnoid seeding of tumor. The incidence of tumor seeding in our series (76.9%) is much higher than in other series. This discrepancy is probably due to the inclusion of a large number of very small tumor metastases that may have been overlooked in other series. In all cases where metastases were observed the primary tumor extended into the cerebrospinal fluid (CSF). Tumor seeding via the cerebrospinal pathway was more frequently associated with malignant tumors. The distribution of tumor metastases correlated with CSF flow and with the site of focal ependymal defects, which were present in normal brains but occurred more frequently and widely in hydrocephalus.
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PMID:Ventricular and subarachnoid seeding of intracranial tumors of neuroectodermal origin--a study of 26 consecutive autopsy cases with reference to focal ependymal defect. 630 22


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