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)

A monoclonal antibody termed "FR77" was obtained from a hybridoma clone established by fusion between P3x63Ag8.653 mouse myeloma cells and spleen cells of a Fischer F344 rat hyperimmune to syngeneic 9L/R3 glioma cells. Immunoperoxidase staining of various cultured cells showed that FR77 was reactive to both rat and human glioma cells, but was not reactive with other nonglioma cells. Immunohistochemical examination of paraffin-embedded or cryostat-frozen sections of various human tissues revealed that FR77 was strongly reactive with glioblastoma, grade III astrocytoma, and craniopharyngioma; partially reactive with intracerebral primitive neuroectodermal tumor, pineoblastoma, and desmoplastic medulloblastoma; and weakly reactive with low-grade astrocytoma. It was not reactive with other types of brain tumors and normal human tissues tested. The FR77-defined antigen was observed to be predominantly localized in the cytoplasm of antigen-bearing cells as suggested by the immunostaining pattern, but part of it was also expressed on the cell surface of glioma cells as demonstrated by a complement-mediated cytotoxic test. Fractionation of the antigenic component and periodic acid treatment of tumor tissue bearing the FR77-defined antigen indicated that the antigen is of a neutral glycolipid nature and that the antigenic determinant to FR77 is present on its sugar portion.
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PMID:Detection of human glioma-associated antigen by rat monoclonal antibody raised against syngeneic rat glioma cells. 376 Sep 59

Laminin is a basement membrane glycoprotein that is expressed in vitro by immature and neoplastic astrocytes. The expression of laminin in vivo was examined immunohistochemically in normal adult brain and 90 neoplasms of the central and peripheral nervous systems. In normal adult brain, laminin was detected in the vasculature, arachnoid, pial-glial membrane, and choroid plexus. The vasculature in all 90 tumors demonstrated intense laminin immunoreactivity. Deposits of laminin were observed at the glioma-mesenchymal junction in several neoplasms, but never between or within neuroepithelial cells. The glial basement membrane often remained intact although surrounded on both sides by invasive glioma or medulloblastoma. However, there was always fragmentation and disruption of the glial membrane in adjacent fields. Laminin expression by tumor cells was observed in 10/10 schwannomas, 9/10 fibroblastic meningiomas, 3/19 nonfibroblastic meningiomas, and 3/6 mixed glioma-sarcomas. Laminin expression in the normal nervous system and in neuroepithelial neoplasms corresponds to regions of recognized basal lamina formation, including the junction between glial and mesenchymal elements. Although invasive gliomas are able to break down the pial-glial basement membrane and gain access to the perivascular or subarachnoid space, this membrane often remains intact late in the invasive process and may represent a partial barrier to tumor invasion. Laminin may be a useful marker for schwannomas, fibroblastic meningiomas, and vascular neoplasms of the nervous system.
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PMID:Immunolocalization of laminin in neoplasms of the central and peripheral nervous systems. 388 47

Using the peroxidase-antiperoxidase (PAP) technique, we examined 35 primary brain tumors for expression of vimentin and GFAP. Both low-grade and high-grade astrocytomas contained vimentin-positive and GFAP-positive cells. Ependymomas also stained for both markers. In gliosarcomas, the glioblastomatous portions stained like astrocytomas, while only vimentin stain was seen in the fibrosarcomatous portions. Medulloblastomas and oligodendrogliomas were negative for both vimentin and GFAP, while meningiomas contained scattered areas of vimentin-positive cells. These results suggest that the expression of vimentin and GFAP is mostly confined to glial-derived tumors, and that vimentin can potentially be a useful marker for distinguishing undifferentiated GFAP-negative glial tumors and mesenchymal tumors from primitive neuroectodermal tumors.
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PMID:Vimentin and glial fibrillary acidic protein in human brain tumors. 388 31

The human glioma-derived cell line D-54 MG and the human medulloblastoma-derived cell line TE-671 have been shown to be sensitive in culture to the pharmacological interference with glutamine metabolism by acivicin, 6-diazo-5-oxo-L-norleucine, and methionine sulfoximine. Using as a guide the multiple contributions of glutamine to the biosynthesis of proteins, purines, and pyrimidines, we now have identified six additional antimetabolites active against these lines in vitro at clinically relevant concentrations. The 50% growth-inhibitory levels of the drugs against D-54 MG in 6-day continuous exposure experiments were: L-asparaginase, 0.057 IU/ml; 5-fluorouracil, 0.5 micrograms/ml; 6-mercaptopurine, 0.8 micrograms/ml; actinomycin D, 0.0007 micrograms/ml; N-phosphonacetyl-L-aspartic acid, 2.3 micrograms/ml; and 5-azacytidine, 0.2 micrograms/ml (3-day exposure. The corresponding 50% growth-inhibitory values in TE-671 were: L-asparaginase, 0.54 IU/ml; 5-fluorouracil, 1.5 micrograms/ml; 6-mercaptopurine, 4.7 micrograms/ml; actinomycin D, 0.00044 micrograms/ml; N-phosphonacetyl-L-aspartic acid, 4.5 micrograms/ml; and 5-azacytidine, 0.49 micrograms/ml. Dipyridamole up to 10 micrograms/ml was inactive against both lines. The isobologram method was used to evaluate the effectiveness of several two-drug combinations which were biochemically designed. The sums of the optimal fractional inhibitory concentrations for the pairs were: acivicin plus L-asparaginase, 0.14; acivicin plus methionine sulfoximine, 0.40; 6-diazo-5-oxo-L-norleucine plus methionine sulfoximine, 0.60; acivicin plus 6-mercaptopurine, 1.0, all in TE-671; and acivicin plus 5-fluorouracil, 0.79, in D-54 MG. Our findings suggest that an antimetabolite regimen exploiting glutamine sensitivity might improve the chemotherapy of some human gliomas and medulloblastomas.
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PMID:Combination chemotherapy in vitro exploiting glutamine metabolism of human glioma and medulloblastoma. 402

Both morphologic and clinical features of 72 consecutive cases of brain tumors, collected over 9 years at Le Bonheur Children's Medical Center, were reviewed. We identified 11 cases as glioblastoma, representing 16% of all intracranial neoplasm and 26% of glial tumors. The patients ranged in age from 1 to 15 years with the median age of 10 years. There were 4 females and 7 males; 2 blacks and 9 whites. The median survival was 9 months. The tumor was observed in both cerebrum and cerebellum. Sexual predominance was not appreciable, although there was male excess. The tumor was significantly more frequent in whites than blacks (p less than 0.05). Similar racial predominance was noted in the other, more common brain tumors in children such as astrocytoma and medulloblastoma.
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PMID:Glioblastoma in children. 409 42

B-mode real-time ultrasound using 5 or 7.5 MHz transducer has been employed during 21 operations for brain pathology and spinal cord lesions. Ultrasonic scanning was performed at the following operations: 10 brain tumors (4 glioblastomas multiforme, 2 astrocytomas, 1 medulloblastoma, 2 metastatic tumors), 2 brain cysts (arachnoid, epidermoid), 1 tuberculous abscess, 3 cerebral hematomas: 2 spinal cord tumors (malignant melanoma, glioma), 2 syringomyelias, 1 posterior longitudinal ligament thickening. Operative ultrasound was useful prior to dural incisions and particularly for subcortical lesions. In addition, ultrasound provided assistance at spinal cord surgery. Our experience has been reviewed and summarized in this report in terms of specific usefulness of assistance of this method which has proven helpful to the neurosurgeons. The types of assistance provided by operative ultrasonography include: Location of dural incision. Localization of brain and spinal cord lesions prior to biopsy. Diagnosis which has not been made preoperatively (e.g. necrosis or cystic area in tumor). Consistency of each lesion (e.g. solid or cystic, necrosis, loculation). Size, extent and depth of brain tumor, cyst, abscess and hematoma. Presence and extent of spinal cord syrinx. Relation of tumor to spinal cord and dura. Access route for biopsy and drainage (avoiding critical areas such as motor strip). Exclusion of bleeding or hematoma following biopsy. Confirmation of the effectiveness of drainage or resection of lesions. Relationship between pathology and surrounding anatomic structures. A number of important assistance by the utilization of ultrasound during neurological surgery have been identified.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Operative ultrasonography of the brain and spinal cord pathology]. 609 Sep 64

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

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

A retrospective study of 366 primary brain tumours in childhood has been carried out, GFAP was detected in juvenile astrocytoma (76/121), adult astrocytoma (34/78), malignant glioma (0/8), other astrocytic tumours (2/4) and medulloblastoma (0/101). In eight medulloblastomas scanty positive cells were seen but were regarded as reactive rather than neoplastic. The presence of GFAP was only found to be of prognostic value in adult astrocytoma, where its occurrence was associated with a more favourable outcome.
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PMID:A study of glial fibrillary acidic protein (GFAP) in childhood brain tumours. 633 23

In 80 specimens of human glioma the production of glial fibrillary acidic protein (GFAP) by tumour cells invading meninges or connective tissue was studied immuno-cytochemically by the PAP technique. In 38 of 55 cases of astrocytoma, glioblastoma, gliosarcoma, and oligoastrocytoma, GFAP immunoreactivity was greater in the invading cells as compared with the main part of the neoplasm. Fifty-eight percent of the astroglial tumours invading the leptomeninges, all astroglial tumours invading connective tissue and all gliosarcomas showed enhanced GFAP immuno-reactivity of tumour cells getting in contact with collagenous tissue, whereas meningeal infiltrates of 25 non-astroglial tumours (oligodendroglioma, ependymoma, medulloblastoma) remained GFAP-negative like the main part of the respective tumours. In the majority of astroglial tumours an increase of GFAP immunoreactivity was found also in perivascular cells of the main part of the tumour. It is concluded that glioma cells are capable of adapting their cytoskeleton to their micro-environment. Contact with dense collagenous tissue appears as an important factor able to induce an increased production of GFAP by adjacent glial cells.
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PMID:Production of glial fibrillary acidic protein (GFAP) by neoplastic cells: adaptation to the microenvironment. 639 Oct 69


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