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)

Immunohistochemically we investigated Rosenthal fibers (RFs) on specimen surgically removed from patients with glioma (three cerebellar astrocytomas, three optic gliomas, two spinal cord astrocytomas, one spinal ganglioglioma). Pathological diagnoses were pilocytic astrocytoma, fibrillary astrocytoma, and ganglioglioma. We utilized sections from the formalin-fixed paraffin-embedded tissues and stained them with H & E, PTAH, PAS as well as with anti-GFAP (glial fibrillary acidic protein) antibody (Ab) and two anti-ubiquitin Abs...anti-PHF (paired helical filament) monoclonal Ab (DF2) which recognizes ubiquitin (H. Mori in Science) and anti-ubiquitin polyclonal Ab provided by Dr. Haas. The primary antibodies were diluted with Tris-saline as follows: anti-GFAP (1:500), DF2 (culture medium without dilution), anti-ubiquitin (2 micrograms/ml). Sections were deparaffinized and incubated with primary antibodies overnight at room temperature. They were visualized by the avidin-biotin-peroxidase complex (ABC) procedure (Vectastain, Vector, USA) and counterstained with hematoxylin. Negative control sections were treated by omitting the primary antibodies. In the representative specimen we compared H & E, anti-GFAP and anti-ubiquitin staining on 3 microcrons serial sections. RFs were eosinophilic (bright red on H & E), purply-stained with PTAH (metachromasia), black with Heidemhein's iron-hematoxylin, and negative with PAS. Anti-GFAP Ab stained glial filaments diffusely in the cytoplasm and cell process of astrocytomas in every case. The peripheral parts of most RFs were intensely stained with anti-GFAP. The whole part of some RFs showed dark staining, and no part of a few RFs showed positive reactivity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunohistochemical study on Rosenthal fibers in gliomas using anti-GFAP and anti-ubiquitin antibodies]. 169 68

A case of ganglioglioma of the optic pathway associated with congenital exophthalmos and strabismus is presented. Since the tumor extended from the right optic nerve to the right geniculate body, it was diagnosed as an optic glioma before operation. However, optic nerve biopsy showed that the lesion was a ganglioglioma. Although a literature review yielded two previous cases of ganglioglioma of the optic pathway, this is the first case in which the tumor involved the whole optic pathway.
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PMID:Ganglioglioma of the optic pathway. A case report. 172 78

The present study determined which oncogenes (N-myc, c-myc, v-sis, or v-fos) were amplified and which messenger ribonucleic acids (mRNA's) accumulated in 10 primary human brain tumors of neuroectodermal origin. The tumors included four glioblastomas multiforme, one mixed glioma (astrocytoma grade I and ependymoma), one astrocytoma grade II, one cystic cerebellar astrocytoma, one ependymoma, one ganglioglioma, and one medulloblastoma. The relative amounts of polyadenylated (poly(A)+) RNA's homologous to these genes and their copy number were determined using the RNA and deoxyribonucleic acid blot hybridization techniques. The N-myc and v-sis probes hybridized strongly to the poly(A)+ RNA from the same recurrent glioblastoma with gene amplifications (N-myc 80 copies; v-sis three to four copies). The c-myc probe hybridized strongly to the recurrent medulloblastoma without gene amplification. The amplification or abundant accumulation of mRNA's homologous to their oncogenes may be involved in tumorigenesis or the aggressiveness of these malignant brain tumors of neuroectodermal origin and may be good molecular indicators of an extremely malignant state in these tumors.
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PMID:Proto-oncogene analyses in brain tumors. 254 Dec 27

The incidence, response to treatment, and outcome of children with pineal region neoplasms is poorly characterized. Since 1975, in one institution, 25 consecutive patients with pineal tumors have undergone biopsy prior to further treatment. This constituted 11% (25/234) of all brain neoplasms seen over this time period. Specific tumors diagnosed included pineal parenchymal tumors ( pineoblastomas , pineocytomas ) in eight patients (32%); germ cell tumors (embryonal cell carcinomas, teratomas, germinomas) in eight patients (32%); glial tumors (astrocytoma, ganglioglioma ) in eight patients (32%); and ganglioneuroblastoma in one patient (4%). Clinical parameters, computed tomographic findings and CSF markers (alphafetoprotein and human chorionic gonadotropin) were unreliable in discriminating between specific tumor types. Response to treatment and patterns of disease relapse were dependent on the type of tumor present. Five of eight children with pineal parenchymal tumors had disease recurrence, and in all leptomeningeal dissemination occurred prior to or concurrent with local relapse. Three of eight children with germ cell tumors and two of eight patients with glial tumors suffered a relapse; in all five children recurrence was initially local. Findings suggest that pineal region neoplasms are not infrequent in childhood; that these tumors vary greatly in histologic type; that contrary to other reports germinomas do not constitute the majority of pineal tumors; and that histologic confirmation is necessary prior to treatment for appropriate management.
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PMID:Pineal region tumors of childhood. 673 22

Gliomas of the optic nerve are rare, comprising only 1% of intracranial neoplasms in adults and 5% in children. This is the first recorded case of a ganglioglioma of the optic nerve. A 2-year-old White boy presented with a convergent squint and blindness of the left eye. At operation a pale, firm, fusiform swelling was found. The cytological and histopathological features are described.
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PMID:Ganglioglioma of the optic nerve. A case report. 685 3

A 35-year-old woman presented with visual hyperacuity and seizures. Radionuclide and CT scans revealed a frontal lobe mass lesion consistent with an astrocytoma. Subtotal removal was necessary due to proximity of the tumor to the motor strip. Initial histopatho logic interpretation was malignant glioma (astrocytoma Grade 2 or 3). Megavoltage irradiation was delivered to a midsagittal dose of 6300 rad in seven weeks. Subsequent review of the slides revealed the tumor to be a microcystic ganglioglioma. The patient is well five and one-half years after treatment. It is important to separate these low grade neoplasms from the more ominous astrocytomas in regard to prognosis after resection and irradiation.
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PMID:Microcystic ganglioglioma treated by partial removal and radiation therapy. 709 89

Gangliogliomas are generally low grade neoplasms composed of mixtures of neoplastic glial and neuronal elements whose origin and exact nature are still controversial. We studied a series of 60 intracranial gangliogliomas looking for coexistent cortical architectural abnormalities (cortical dysplasia, microdysgenesis) and to determine if tumor behavior correlates with MIB1 (marker of cellular proliferation) labeling. The patients included 34 males and 26 females who ranged in age from 6 months to 55 years (mean 20 years). Thirty-eight tumors (63%) were located in the temporal lobe and 6 (10%) in the frontal lobe. Fifty-four patients (90%) presented with seizures (most with intractable epilepsy) and the duration of seizures ranged from 1 to 38 years (mean 14 years). In all cases, the predominant glioma component resembled a low grade fibrillary astrocytoma. In 14 tumors (23%), an oligodendroglial component was present. In one case, the glial component resembled an anaplastic astrocytoma. The tumors were characterized variously by perivascular chronic inflammation (N = 45, 75%), vascular proliferation (N = 36, 60%), granular bodies (N = 54, 90%), binucleated neurons (N = 36, 60%), calcification (N = 28, 47%), and cystic degeneration (N = 26, 43%). Meningeal involvement by tumor was observed in five (8%) cases. In 38 patients, sufficient tissue was resected to evaluate for the presence of concomitant cortical architectural abnormalities. Cortical architectural abnormalities were identified near to but clearly separate from the tumor in 19 (50%) patients. Only four patients including the anaplastic tumor died with tumor progression. MIB1 indices (positive tumor cells/1,000 tumor cells counted) in 54 cases ranged from 0 to 10.2 (mean 1.1 +/- 1.0).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cortical architectural abnormalities and MIB1 immunoreactivity in gangliogliomas: a study of 60 patients with intracranial tumors. 754 47

We identified 39 patients with chronic epilepsy (seizures > or = 2 years) proven to have primary brain tumors. These cases represent approximately 12% of the surgery cases for epilepsy in the same period. Mean age of seizure onset was 13.2 years: mean duration before operation was 10.5 years. Thirty-eight of 39 had normal neurologic examination. Twenty-six tumors were temporal, 7 were frontal, 4 were parietal, and 2 were occipital. Nine of 26 (34.6%) of the temporal group had contralateral interictal EEG spikes. Pathology was 15 ganglioglioma, 13 low-grade astroctoma, 4 oligodendroglioma, 2 low-grade mixed glioma, 1 pleomorphic xanthoastrocytoma, 2 dysembryoplastic neuroepithelial tumor, and 1 ependymoma. Postoperative seizure frequency (minimum follow-up 6 months) ranged from 15 to 16 seizure-free auras only in patients with temporal tumors and total gross tumor removal (mean follow-up 28 months) to 0 of 6 seizure-free in patients with extratemporal tumors who underwent subtotal resection or biopsy.
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PMID:Chronic intractable epilepsy as the only symptom of primary brain tumor. 824 54

Histopathological features that suggest the diagnosis of ganglioglioma require, in most cases, confirmation by special stains to distinguish these tumors from other gliomas. For this purpose, immunostaining for synaptophysin, which has previously been shown to selectively label the cell surface of neoplastic ganglion cells, was used to retrospectively examine glioma tumor specimens. Sixty-three cases of ganglioglioma were identified. The files of the Division of Neuropathology of New York University Medical Center contained 45 tumors that had been diagnosed as ganglioglioma, of which 42 were verified by synaptophysin; three cases were reclassified, two as astrocytomas and one as a gangliocytic paraganglioma. Thus, a tumor identified as ganglioglioma based on other criteria was likely to be a ganglioglioma. The other 21 cases of gangliogliomas were originally diagnosed as astrocytoma or mixed glioma, but were shown by synaptophysin staining to be gangliogliomas. In some cases the ultimate diagnosis was obtained after radical surgery provided relatively abundant amounts of tissue, thereby limiting sampling errors, in contrast to the biopsies from which the original diagnoses were made. Histopathological review of these cases demonstrated that four features represent important clues to the correct diagnosis: 1) clusters of large cells potentially representing neurons (without such cells the tumor cannot be classified as a ganglioglioma); 2) no perineuronal clustering of the glial cells around the alleged neoplastic neurons; 3) fibrosis (desmoplasia); and 4) calcification. Binucleate neurons, previously suggested to be common in gangliogliomas, were not frequently found in this series, and lymphocytic infiltrates, while common, are so often found in other tumors that they gave no specific hint that any single neoplasm was a ganglioglioma. The glial elements were astrocytic in all cases, except that one tumor also had oligodendroglial and ependymal patterns. Four tumors also had small mature neurons, as seen in neurocytomas. Cells from one tumor were successfully grown in short-term tissue culture; the culture contained large dividing neurons with synaptophysin immunoreactivity as well as smaller dividing cells, demonstrating that the neuronal cells are a proliferating element in gangliogliomas.
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PMID:Central nervous system gangliogliomas. Part 1: Pathology. 824 54

The new edition of the World Health Organization (WHO) book on 'Histological Typing of Tumours of the Central Nervous System' reflects the progress in brain tumour classification which has been achieved since publication of the first edition in 1979. Several new tumour entities have been added, including the pleomorphic xanthoastrocytoma, central neurocytoma, the infantile desmoplastic astrocytoma/ganglioglioma, and the dysembryoplastic neuroepithelial tumour. The list of histological variants has also been expanded. In line with recent morphological and molecular data on glioma progression, the glioblastoma is now grouped together with astrocytic tumours. The classification of childhood tumours has been largely retained, the diagnosis primitive neuroectodermal tumour (PNET) only being recommended as a generic term for cerebellar medulloblastomas and neoplasms that are histologically indistinguishable from medulloblastoma but located in the CNS at sites other than the cerebellum. The WHO grading scheme was revised and adapted to new entities but its use, as before, remains optional.
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PMID:The new WHO classification of brain tumours. 829 85


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