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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regional blood-to-tissue transport, expressed as a unidirectional transfer rate constant (K), was measured in experimental brain tumors using alpha-aminoisobutyric acid (AIB) labeled with carbon 14 and quantitative autoradiography. A total of sixteen oligodendrogliomas, four mixed gliomas, three astrocytomas, two diffuse gliomatosis, one anaplastic astrocytoma, one ependymoma and four malignant schwannomas were studied in 9 rats. The mean Ks for all glioma classifications were similar, averaging 2.6 +/- 0.4 (standard error of the mean) ml . kg-1 . min-1, and were only slightly higher than those for nontumorous parietal cortex (2.1 ml . kg-1 . min-1), corpus callosum (0.9 ml . kg-1 . min-1), and a comparable region of brain tissue in the contralateral hemisphere (1.3 ml . kg-1 . min-1). Values of K varied minimally in the intracerebral gliomas and were marginally correlated with tumor cell morphology in only two tumors. In some (but not all) of the larger gliomas, increased vascularity, with or without endothelial proliferation, was associated with a 3- to 15-fold increase in K. Regional K values in malignant schwannomas were highly variable (4 to 207 ml . kg-1 . min-1) and generally were not correlated with specific histological features of the tumor, except in some regions with increased vascularity. Estimates of the average fractional extraction of AIB by the intracranial gliomas and malignant schwannomas were 0.01 and 0.2, respectively; average fractional extractions for nontumorous brain were approximately 0.003.
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PMID:Regional blood-to-tissue transport in ethylnitrosourea-induced brain tumors. 662 37

A number of neural and nonneural tumor cell lines of rat and human origin were assayed for neuron-specific enolase (NSE) by radioimmunoassay. Most neural tumor cell lines had appreciably higher levels of NSE than did the nonneural tumor cell lines, the highest levels being found in two anaplastic rat glioma lines ( F98 and T24). These two lines contained more than twice the amount of NSE found in a rat pheochromocytoma line (PC12) and in neuroblastoma lines derived from rats ( B35 and B50 ) or humans (IMR-32 and SHSY - 5Y ). Several of the rat glioma and schwannoma lines were inoculated intracerebrally into syngeneic rats. In the resulting tumors, NSE was demonstrable by immunohistochemistry only in those from the F98 and T24 cell lines. A number of ethylnitrosourea-induced rat tumors were also examined immunohistochemically for NSE: NSE was demonstrated in three anaplastic gliomas; three astrocytomas; and two mixed gliomas. Reactive astrocytes were also positive. Fibroadenomas of apocrine and mammary glands in rats were weakly positive, but other extraneural tumors tested were negative. Since normal neuronal elements, axonal swellings, and amine precursor uptake and decarboxylation cells are strongly positive for NSE, whereas glia and most other normal cells are negative, we hypothesize that the elevated metabolic demands imposed on neoplastic and reactive glial cells and on some extraneural tumors necessitate the opening up of metabolic pathways that are normally operative only in neurons and neuroendocrine cells, therefore resulting in the synthesis of the more stable neuron-specific form of enolase.
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PMID:Immunoradiometric and immunohistochemical demonstration of neuron-specific enolase in experimental rat gliomas. 672 96

To provide the significance of LDH isozymes in rat CNS tumors, the changes in lactic dehydrogenase isozyme and calculated ratios of H- to M- subunit were studied by means of polyacrylamide gel enzymoelectrophoresis in tumor extracts from CNS tumors (7 astrocytomas, 4 oligodendrogliomas, 7 mixed gliomas, 6 anaplastic gliomas, 3 glioependymomas, 1 astroblastoma, 11 neurinomas, 8 anaplastic neurinomas and 1 meningioma in Wistar rats which were induced by ethylnitrosourea). The isozyme patterns were compared to those obtained from normal rat CNS tissues. Among the glioma group, oligodendroglioma showed the highest H/M ratio followed by mixed glioma, glioependymoma, astrocytoma, astroblastoma and anaplastic glioma in order of decreasing of H/M ratios. On the other hand, the H/M ratio of neurinoma was significantly higher than that of anaplastic neurinoma. These observation suggested that determination of LDH isozyme patterns could supplement the histological evaluation of brain tumors.
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PMID:LDH isozyme analyses of ethylnitrosourea-induced central nervous system tumors in rats. 739 14

The frequent allelic loss of chromosome 19q in human gliomas suggests that 19q harbors a tumor suppressor gene that is integral to glioma tumorigenesis. Our initial deletion mapping of this gene localized the common region of deletion to the distal long arm, 19q13.2-13.4. To bracket the putative tumor suppressor gene further, we have studied this region in 55 gliomas, using loss of heterozygosity studies for 11 well mapped, highly informative microsatellite polymorphisms that cover this area: D19S178; BCL3; APOC2; ERCC1; DM; D19S112; HRC; D19S246; KLK; D19S180; and D19S254 (from centromeric to telomeric). Twenty astrocytic, oligodendroglial, and mixed gliomas had deletions affecting this region. Of nine partial deletions, two cases maintained heterozygosity at APOC2 while showing allelic loss at the more telomeric markers, ERCC1 and DM, while five cases maintained heterozygosity at HRC but lost the more centromeric markers, D19S112 and DM. Nine cases lost the entire D19S178 to D19S254 region. Three astrocytic gliomas, including one with an interstitial deletion, had terminal deletions of 19q13.4. The minimum area of overlap shared by the interstitial deletions is between APOC2 and HRC, including ERCC1, DM, and D19S112. These findings suggest that the glioma tumor suppressor gene maps to an approximately 8-cM/5-megabase region on 19q13.2-13.3 between the proximal marker APOC2 and the distal marker HRC. Among the DNA repair/DNA metabolism genes on chromosome 19q, ERCC1, LIG1, and perhaps ERCC2 are within the common area of deletion; XRCC1 is centromeric and is therefore excluded as a candidate.
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PMID:The putative glioma tumor suppressor gene on chromosome 19q maps between APOC2 and HRC. 806 76

Neoplastic transformation occurs in all glial cell types of the human nervous system, producing a wide variety of clinico-pathological entities and morphological variants. Astrocytomas are most common and span an unusually wide spectrum, ranging from the slowly growing juvenile pilocytic astrocytoma to the highly malignant glioblastoma multiforme. Diffusely infiltrating astrocytomas of the cerebral hemispheres show an inherent tendency for progression towards a more malignant phenotype. This change is morphologically categorized in histologic grading schemes (e.g., WHO Grade II to IV) and is associated with the sequential acquisition of genetic alterations, including mutations in the p53 and homozygous deletions of the p16 tumour suppressor genes. Loss of heterozygosity on chromosomes 10 and 19q as well as amplification of the EGF receptor are largely restricted to malignant gliomas and thus considered late events in astrocytoma progression. Gliomas often show phenotypic expression of different glial cell lineages (e.g., oligoastrocytoma). Recent studies suggest that the occurrence of mixed gliomas is not indicative of a polyclonal origin but rather reflects altered gene expression, leading to a change in the balance of growth factors influencing glioma differentiation.
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PMID:Histopathology, classification, and grading of gliomas. 858 58

The past few years have seen remarkable progress in understanding the molecular genetic basis of glioma formation. Affected oncogenes and tumor suppressor genes have been identified and putative tumor suppressor loci have been mapped. These studies have illustrated distinct molecular pathways for different glial neoplasms. We summarize the findings of an ongoing study initiated to characterize human gliomas on a molecular basis. The data are compiled from 150 astrocytic, oligodendroglial, and mixed gliomas that were assessed for genomic alterations characteristic of these neoplasms, i.e., loss of portions of chromosomes 1p, 9p, 10, 17p, 17q, and 19q, mutations of the p53 tumor suppressor gene, and amplification of the EGF receptor (EGFR) gene. Our findings support the hypothesis that distinct genetic pathways result in the formation of astrocytic and oligodendroglial neoplasms of different malignancy grades, and that glioblastoma multiforme may be subdivided into genetically distinct subsets. Such findings may not only lead to a better understanding of neoplastic transformation in glial cells, but may also have a major impact on clinical neuro-oncology.
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PMID:Molecular pathways in the formation of gliomas. 858 67

Based on in vitro studies which demonstrate that collagen IV and laminin inhibit the proliferation and invasiveness of glioma cells, we investigated the clinical significance of these extracellular matrix proteins (ECM) in patients with gangliogliomas, tumors in which ECM is often a prominent feature. Our study compared the relative presence and deposition pattern of collagen IV and laminin in 19 gangliogliomas and in 18 gliomas without ganglion cell differentiation (8 low-grade astrocytomas, 7 anaplastic astrocytomas, and 3 anaplastic mixed gliomas). We also examined whether the presence of collagen IV and laminin correlated with other features often observed in gangliogliomas, including perivascular lymphocytic inflammation, granular bodies, microcalcification, and subarachnoid extension, and whether any of these features were associated with the patient's clinical course. Significant deposition of collagen IV and laminin was found in 9 gangliogliomas (47%), but in none of the other gliomas. The presence of these extracellular proteins in gangliogliomas correlated with both perivascular inflammation (P = 0.003), and involvement of the leptomeninges by tumor (P = 0.008). The duration of symptoms prior to surgical resection was significantly longer for patients whose tumors showed extracellular deposition of collagen IV and laminin than for patients whose tumors lacked deposition of these proteins (mean 13.7 vs 5.1 years; P = 0.02). In addition, the duration of symptoms was significantly longer for patients whose tumors exhibited perivascular inflammation than for patients whose tumors displayed little or no perivascular inflammation (mean 14.8 vs 4.8 years; P = 0.01). These findings suggests that collagen IV and laminin and perivascular inflammation are related to the indolent behavior of gangliogliomas.
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PMID:The clinical significance of extracellular matrix in gangliogliomas. 895 48

18 cases of low-graded mixed gliomas were studied using the two lectins Concanavalin A (Con A) and Peanut lectin (PNA). Con A stained cytoplasm and processes of tumoral astrocytes, whereas PNA stained cell membranes of tumoral oligodendrocytes. Con A and PNA are reliable markers for astrocyte and oligodendrocyte areas of mixed gliomas, respectively. A part of cells were overlappingly positive for both lectins. They expressed an oligosaccharide pattern of both glioma types and represented a third, intermediate cell type of mixed gliomas. The existence of intermediate cells close to astrocytic and oligodendroglial cell types in mixed gliomas could result from transformation processes of neoplastic glial cells or from the malignant transformation of a common glial precursor cell.
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PMID:Lectinhistochemistry of mixed gliomas demonstrating an intermediate cell type. 947 36

Anaplastic mixed gliomas are rare tumors that occur mostly in the cerebral hemispheres. They have a distinctive histological appearance characterized by the presence of two or more glial cellular constituents. The incidence of malignant mixed glioma of the brainstem and posterior fossa is extremely low. The authors report an unusual case of an exophytic malignant mixed glioma. Following subtotal resection, the patient received conventional radiotherapy, but continued to deteriorate, and died five months after surgery. The extensive literature review focuses on histopathology, clinical features, natural history, and possible treatment modalities of this unusual neoplasm.
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PMID:Exophytic malignant brainstem mixed glioma in an adult: a case report. 952 90

The histologic determination of the degree of tissue anaplasia and grade of malignancy of gliomas is based upon qualitative histological features (nuclear pleomorphism, mitoses, endothelial proliferation, tumor necrosis). This grading approach is influenced by the subjective interpretation of the pathologist, especially concerning the weighting of criteria (scant, moderate, pronounced). An observer-independent approach seems to be feasible by abandoning the concept of parameter weighting in favor of an binary approach noting only the presence or absence of these structure parameters. This grading procedure is recognized in the revised WHO classification of brain tumors for common type astrocytomas (Ste. Anne-Mayo System, SAMS). Our results indicate that a similar approach is also suitable for grading purposes of oligodendrogliomas and mixed gliomas. Our recent investigations on glioma grading showed, both for astrocytomas and oligodendrogliomas, that a two-tiered grading scheme distinguishing only "low-grade" and "high grade" cases was prognostically relevant. For all glioma entities the onset of tumor angiogenesis with endothelial proliferation and contrast enhancement in CT and MRI seems to be the key criterion indicating irreversible tumor progression to the "high" malignancy grade.
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PMID:[Grading of astrocytomas and oligodendrogliomas]. 974 10


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