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)

An autopsy case of glioblastoma of the cerebellum associated with an intracerebellar hemorrhage and showing CSF seedings is reported. A 26 year-old male was admitted to our hospital with a 10-day history of headache, nausea and vertigo. On admission, disturbance of consciousness (10-20 by JCS), irregular respiration and central fixation of both eyes suggesting increased intracranial pressure and early stage of central herniation were recognized clinically. The cerebellar signs of dysmetria and nystagmus were also observed. CT scan and angiography revealed an avascular large mass in the right cerebellar hemisphere, obstructive hydrocephalus and upward transtentorial herniation. On MRI study, the mass was demonstrated to be a subacute hematoma with a small tumor in its margin. Total removal of the tumor and aspiration of the hematoma were performed. Histological examination revealed a highly cellular and pleomorphic astrocytic tumor with scattered small necrosis and glomeruloid capillary endothelial proliferation, typical of glioblastoma multiforme. During postoperative radiochemotherapy (focal irradiation to the posterior fossa), the tumor showed rapid regrowth and a second look operation was performed. He was readmitted 3 weeks after radiochemotherapy with complaints of severe headache, nausea and lumbago. He then suddenly became dyspnea, tetraplegic and bradycardic. Neuroradiological investigation revealed multiple masses in the suprasellar region, medulla oblongata and the cervical spinal cord, but no recurrence in the cerebellum. Malignant cells were noted on CSF cytology. During chemotherapy for CSF tumor dissemination, his condition deteriorated rapidly and he died 7 months after the onset of symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Glioblastoma of the cerebellum: report of an autopsy case associated with intratumoral hemorrhage and CSF seedings]. 165 2

'Gliosarcomas' have long been considered to be mixed gliomas and sarcomas. The present study failed to define criteria which clearly delineate 'gliosarcomas' from glioblastoma multiforme and suggests that 'gliosarcomas' should be considered as spindle cell glioblastomas. A total of six cases originally diagnosed as 'gliosarcomas' were compared with four cases of glioblastoma multiforme. No clinical or prognostic features were defined which would clearly separate 'gliosarcomas' from glioblastoma multiforme. Macroscopically, biopsies from 'gliosarcomas' ranged from firm, apparently well-circumscribed tumours to poorly circumscribed lesions with a soft consistency resembling glioblastoma multiforme. Histology revealed a continuous spectrum in which 'gliosarcomas' with large reticulin-rich areas of spindle cells merged with typical glioblastomas containing only small islands of spindle cells and reticulin staining. Immunocytochemistry for glial fibrillary acidic protein (GFAP); S100 protein and alpha-smooth muscle actin (ASMA) showed that the majority of cells in reticulin-poor areas of 'gliosarcoma' and glioblastomas expressed S100 protein and GFAP; many expressed ASMA and some expressed both GFAP and ASMA. Spindle cells in reticulin-rich areas of 'gliosarcomas' and glioblastomas most frequently expressed ASMA but many cells also expressed S100 protein and GFAP; some cells expressed both GFAP and ASMA. The results of this study and a review of the literature suggests that there is a clinical, radiological and pathological continuum with glioblastoma and 'gliosarcoma' at different ends of the spectrum. It is suggested, therefore, that most, if not all, 'gliosarcomas' be redesignated as spindle cell glioblastomas and not be considered as a mixture of glioma and sarcoma.
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PMID:Spindle-cell glioblastoma or gliosarcoma? 162 Feb 80

The case of a 42-year-old man with a cerebral glioblastoma multiforme associated with marked neovascularization of the arachnoid of the brain stem and spinal cord is reported. All of the neurological symptoms and signs were referrable to the glioblastoma and resultant craniotomies. The arachnoid contained a proliferation of well differentiated blood vessels. This neovascularization occurred in the absence of local tumor or inflammation. We suggest that the neovascularization resulted from release of a tumor angiogenesis factor into the cerebrospinal fluid.
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PMID:Distant angiogenesis in a patient with glioblastoma multiforme. 169 77

Immunohistochemistry was performed on paraffin sections from human glioblastoma multiforme and normal brain tissue. Acidic fibroblast growth factor (FGF) was abundantly present in astrocytes from all glioblastomas studied. Basic FGF was found in the matrix surrounding proliferating blood vessels in most of the glioblastomas. In contrast, astrocytes from normal brain did not contain acidic FGF, and perivascular matrix staining was not demonstrated for basic FGF in the normal brain. Both growth factors could be demonstrated in neurons, Purkinje cells, capillary endothelium, and arterial walls in the normal brain. This study implicates both growth factors in the pathogenesis of malignant glioma. Both may be significant mediators of angiogenesis in glioblastoma.
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PMID:Acidic and basic fibroblast growth factors are present in glioblastoma multiforme. 171 53

Glioblastoma multiforme, the most malignant astroglial-derived tumor, grows as an adherent mass and locally invades normal brain. An examination of adult cerebral glioblastoma biopsy material for the expression of adhesive proteins that might potentiate adhesion and invasion demonstrated tumor cell-associated vitronectin (5/5). In contrast, vitronectin was not detected associated with glial cells in low grade astroglial tumors (0/4), reactive astrogliosis (0/4), or in normal adult cortex and cerebral white matter (0/5). Also, a wide variety of other adhesive ligands were absent from the glioblastoma tumor parenchyma. The alpha v beta 3 integrin was the only vitronectin receptor identified in glioblastoma tumors in situ, and was also not expressed on low grade astroglial-derived tumors, reactive astrogliosis, or on glia or neurons in normal adult cortex and cerebral white matter. In a cell attachment assay, cultured glioblastoma cells attached to the parenchyma of glioblastoma tumor cryostat sections at the sites of vitronectin expression, but failed to attach to normal brain. This adhesion was inhibited by antibodies directed against vitronectin, the alpha v beta 3 integrin, and with an Arg-Gly-Asp-containing peptide. These data provide evidence for a cell adhesion mechanism in glioblastoma tumors that might potentiate glioblastoma cell invasion of normal brain.
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PMID:Glioblastoma expression of vitronectin and the alpha v beta 3 integrin. Adhesion mechanism for transformed glial cells. 172 25

Gliomas are the most common tumors in the brain and are almost always malignant in adults. The most malignant and most common glioma is glioblastoma multiforme. Median survival of patients with glioblastoma is less than 20 months following treatment. This poor prognosis reflects the limited efficacy of the currently available treatment modalities. Therefore, many attempts have been made to improve the treatment of this lethal disease. This paper reviews the progress that has been made recently in the treatment of malignant glioma with a focus on studies reported during the last year.
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PMID:Treatment of gliomas in adults. 189 16

The authors report on two cases of multicentric glioblastoma multiforme, one of them being a trilocular glioblastoma, whereas in the second case a second focus developed contralaterally. Both patients received whole skull radiation of 40 Gy. The patient who suffered from the primarily unilocal tumour was given a tumour boost. The article reports on the imaging via CT and MR.
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PMID:[The multicentric glioblastoma multiforme]. 196 94

A large-animal model was developed to facilitate the noninvasive investigation of the effect on the human glioma-derived D-54 MG (glioblastoma multiforme) continuous cell line of a variety of therapeutic regimens. Twenty random-bred male cats were inoculated intracerebrally with 1 x 10(7) D-54 MG tumor cells after being initiated on one of three preparatory regimens of cyclosporin A p.o. Reproducible success of D-54 MG xenotransplantation (100%, 6 of 6 cats) was achieved only after pretreatment with 120 mg cyclosporin A p.o. (24-30 mg/kg) daily for greater than or equal to 10 days prior to tumor implantation. High-performance liquid chromatography-derived whole blood cyclosporin A 12-h trough levels of greater than or equal to 640 ng/ml were seen in successful implants. Lesions ranging from 2 to 20 mm in diameter were seen in cats sacrificed 27-44 days after implantation with no growth seen in control animals. Histopathological examination revealed the tumors to be well-circumscribed anaplastic intracerebral tumors with some invasion into surrounding host parenchyma. Perivascular lymphocytic cuffing was observed, but intratumoral lymphocytic infiltration was minimal. Gadolinium-EDTA-enhanced nuclear magnetic resonance imaging provided accurate tumor localization in T1-weighted images (TE 26 ms; TR 600 ms). Biochemical tests of kidney, liver, and hematological function were within normal limits, although 10% (2 of 20) of the animals developed gingival hyperplasia, and 5% (1 of 20) developed intussusception. The reproducible growth of the D-54 MG human glioblastoma cell line in a large-animal model eliminates many of the limitations associated with the standard nude mouse/rat model, thereby providing a novel test bed for a variety of imaging modalities as well as for drug immunoconjugate localization and toxicity studies.
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PMID:Development of a large-animal human brain tumor xenograft model in immunosuppressed cats. 201 4

Reported are three cases of a spinal leptomeningeal dissemination from supratentorial malignant gliomas, in which the recurrence of the primary tumors of the intracranial leptomeningeal involvement was not observed clinicopathologically. All cases complained of spinal cord symptoms such as paraplegia or a sensory disturbance from time to time after the initial operation for their intracranial primary tumors. The duration between the first operation and the appearance of the spinal cord symptoms ranged from 11 to 17 months. In all cases, a computerized tomography scan demonstrated no recurrence of the primary tumor and no findings indicating intracranial leptomeningeal gliomatosis, such as a diffuse contrast enhancement of the ventricular wall or the subarachnoidal space, or hydrocephalus. Myelography showed a block or an irregular filling defect in two cases given immediate operations for spinal mass lesions. In one of these cases, a well-defined extramedullary tumor was removed at the level of the 7th-8th thoracic vertebrae. The pathological diagnosis was a glioblastoma multiforme, which was similar to the primary tumor. The patient survived for 18 months after total removal of the spinal tumor followed by postoperative spinal irradiation. All patients died of recurrent tumors from 3 to 18 months (mean: 8 months) after the appearance of the spinal cord symptoms. In the other case, an intramedullary tumor was found by a laminectomy. These two cases were autopsied. In one, an intramedullary tumor was found to extend from the lower medulla oblongata to the cervical cord, whereas the recurrence of the primary tumor was not seen and there was no intracranial leptomeningeal invasion nor any spinal subarachnoid seeding. The pathological diagnosis of this intramedullary tumor was a glioblastoma. In the other, there was a diffuse leptomeningeal dissemination of glioblastoma multiforme throughout the spinal cord, with an intramedullary invasion to almost all parts. A partial intracranial subarachnoid seeding of a malignant lower grade tumor than seen in the spinal lesion was found, though there was no recurrence of the primary tumor.
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PMID:[A clinicopathological study of the spinal leptomeningeal dissemination from cerebral malignant gliomas without a recurrence of the primary lesions]. 215 48

Localization and characterization of endothelin receptors in surgical specimens of human gliomas (6 benign astrocytomas and 7 glioblastomas multiforme) and in normal human cortices were studied using quantitative receptor autoradiographic methods. Low numbers of [125I]endothelin-1 [( 125I]ET-1) binding sites were detected in the gray matter of the human frontal cortex, with little binding in the white matter. Conversely, relatively high numbers of [125I]ET-1 binding sites were homogeneously present in tissue sections derived from astrocytomas, whereas higher numbers of [125I]ET-1 binding sites were heterogeneously located on groups of cells with a pseudopalisading appearance and pleomorphic astrocytes in glioblastoma multiforme. Necrotic areas within the tissue sections derived from glioblastoma were devoid of binding. Binding of [125I]ET-1 to gliomas and normal gray matter was specific. Unlabeled ET-1 and its natural analogs (ET-2 and ET-3) inhibited the binding of [125I]ET-1 to these lesions in a concentration-dependent manner and with similar high potencies. Possibly related substances, such as ion channel regulators (omega-conotoxin, apamin, and tetrodotoxin), a Ca2+ channel blocker (nicardipine), and growth factors (epidermal growth factor and insulin-like growth factor I), did not affect the binding to tissue sections derived from gliomas or from normal frontal cortices. Scatchard analysis revealed the presence of a single class and high-affinity binding sites for endothelin in normal cortex and in gliomas. There was no significant difference in the binding affinities: dissociation constants (Kd) were 2.1 +/- 0.5 nM in 6 astrocytomas, 2.5 +/- 0.4 nM in 7 glioblastomas, and 1.4 and 1.5 nM in two normal cortices.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Localization and characterization of endothelin receptors in human gliomas: a growth factor? 216 28


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