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

Morphologically distinct virus-like particles (VLP), similar to R-type VLP, were observed by electron microscopy in experimental rat central nervous system tumors induced with the B-77-C strain of avian sarcoma virus (ASV). R-type VLP have a characteristic internal radial structure and were observed previously only in hamster cells and in an established bovine cell line. They were not observed in the B-77 ASV inoculum used to induce the rat tumors or in the B-77 induced hamster glioma cells from which the B-77 was rescued. Nevertheless, the genome of an endogenous hamster R-type particle also might have been rescued and carried in the B-77 inoculum. Alternatively, R-type VLP may exist in a number of animal species, including the rat, and may be expressed in certain conditions such as neoplastic transformation.
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PMID:R-type virus-like particles in avian sarcoma virus-induced rat central nervous system tumors. 16 94

A comparative analysis was performed on the electrophysiological properties of 11 neoplastic neurogenic cell culture lines and five other cell lines of different origin (HV1C, rat bile duct carcinoma; BICR/M1RK, rat mammary tumor; HeLa, human cervix carcinoma; 3T3, mouse embryo; REe, rat embryo). Neurogenic lines were derived either from N-ethyl-N-nitrosourea-induced neoplasms of the nervous system or from cultured fetal rat brain cells that had undergone neoplastic transformation in vitro after exposure to N-ethyl-N-nitrosourea in vivo. Electrical membrane excitability was lacking in all neurogenic cells analyzed. Their membrane potential and input resistance values were similar to those of the nonneurogenic lines. Intercellular ionic coupling was consistently observed between cells of a fibroblastoid shape or cells bearing multiple cytoplasmic processes (i.e., all neurogenic lines HV1C, BICR/M1RK, and 3T3). Epithelioid cells (i.e., HeLa, REe, an NV1C subpopulation, and a GV1C1 variant) showed no such intercellular communication. In vivo monolayer cultures on glass coverslips were obtained by a modified i.p. diffusion chamber technique. Under these conditions, the cells (with the exception of a glioma-derived cell line) retained the morphological appearance and electrophysiological properties observed in vitro.
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PMID:Electrophysiological properties of ethylnitrosourea-induced, neoplastic neurogenic rat cell lines cultured in vitro and in vivo. 17 99

We have recently reported that fetal BD IX-rat brain cells (FBC), transferred to long-term culture after a transplacental pulse of EtNU on the 18th day of gestation, undergo neoplastic transformation in vitro ("BT-cell lines"). Tumors developed upon s.c. reimplantation of BT-cells into baby BD IX-rats, appeared histologically as neurinoma-, glioma- or glioblastoma-like, and frequently as pleiomorphic neoplasms. In spite of a more atypic cellular morphology, these tumors grossly resembled the different types of neuroectodermal rat neoplasms induced by EtNU in vivo. Like the neoplastic cell culture lines derived from EtNU-induced, neuroectodermal BD IX-rat tumors ("V-cell lines"), the BT-lines contained multipolar glia-like cells, but also flat cells with fewer and shorter cytoplasmic processes, and occasionally giant cells. Both the V- and BT-lines showed different levels of aneuploidy. They contained multiple subpopulations of cells, as reflected, e.g., by plurimodal pulse-cytophotometric DNA distributions. All lines contained, to varying degrees, the nervous system-specific protein S-100, a "marker" not yet expressed in FBC. There was no indication of more than borderline neurotransmitter activity, suggesting that proliferating (precursor) cells of glial lineages may preferentially undergo malignant transformation after exposure to EtNU during this stage of brain development.
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PMID:Phenotypic properties of neoplastic cell lines developed from fetal rat brain cells in culture after exposure to ethylnitrosourea in vivo. 19 83

Experimental animal models resembling most human brain tumor types can be induced by exposure to oncogenic viruses or chemical carcinogens: Astrocytomas and glioblastoma multiforme can be produced experimentally by intracerebral injection of oncornaviruses, whereas medulloblastomas, choroid plexus papillomas, and ependymomas can be induced by the papovaviruses. Adenoviruses have been utilized to cause medulloepitheliomas, neuroblastomas, and retinoblastomas. All three groups of viruses can result in sarcoma production. Gliomas represent the primary tumor type induced in the brain by chemical carcinogens. These autochthonous tumor systems are reviewed, with emphasis on methods, tumor type, latency period, advantages, and disadvantages. In addition, recent investigations of molecular events involved in neoplastic transformation by chemical carcinogens are summarized.
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PMID:Chemical- and virus-induced brain tumors. 20 37

Immunohistochemical analysis of intermediate filament (IF) proteins was performed on frozen sections of 16 childhood glial tumors using a library of 10 antigen-specific IF protein directed monoclonal antibodies (MoABs) and a four-step biotin-streptavidin-alkaline phosphatase conjugated antigen detection immunocytochemical technique. Human glial fibrillary acidic protein (GFAP) and vimentin were expressed in all brain tumors. High molecular weight (200 kDa) neurofilament (NF-H) protein was expressed in 15 out of 16 tumors; medium molecular weight (160 kDa) neurofilament (NF-M) in seven out of 16 tumors; and low molecular weight (68 kDa) neurofilament (NF-L) in five out of 16. Positive acidic keratin reactivity was found in five out of 16 tumors using MoAB AE1. Expression of a keratin pair was detected with MoAB AE2 in five out of 16 tumors. A second keratin pair in 14 out of 16 glial tumors was demonstrated with MoAB AE3. Immunostaining with AE5 defined the expression of another basic keratin (64 kDa) in nine out of 16 glial tumors. Finally, in 14 out of 16 astrocytomas an individual 51 kDa acidic keratin (detected with MoAB AE8) was expressed. Glial tumor cells contain cell lineage specific and nonspecific IF proteins in the following IF pattern: AE3+, AE8+, GFAP+, vimentin+, and NF-H+. The heterogenous composition of these cytoskeletal IF proteins in childhood glial tumors may reflect a direct stage dependent correlation with their neoplastic transformation.
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PMID:Co-expression of four intermediate filament subclasses in childhood glial neoplasms. 172 88

Monoclonal antibodies (MAb; DMAb, monoclonal antibodies derived at Duke Medical Center) directed against the oncofetally expressed lactotetraosyl gangliosides 3'-isoLM1 (IV3NeuAc-LcOse4Cer) and 3',6'-isoLD1 (IV3NeuAc,III6NeuAc-LcOse4Cer) were produced and their reactivity spectra compared to that of the alpha-3'-isoLM1 MAb SL-50. The IgM MAb SL-50 defines the epitope NeuAc (or NeuGc)alpha 2-3Gal beta 1-3GlcNAc, the terminal sequence of both gangliosides. SL-50 requires an unsubstituted GlcNAc residue; IgM DMAb-14 will accept the alpha 2-6 linked sialic acid to GlcNAc found in 3',6'-isoLD1. Immunohistochemical localization of 3'-isoLM1 was performed on 31 biopsy specimens of human gliomas; 15 (48%) expressed 3'-isoLM1 as defined by binding of MAb SL-50. Staining of small anaplastic cells, giant cells, and the glial component of gliosarcomas was observed. Neoplastic gemistocytes, when present, showed particularly intense staining. The 3'-isoLM1 and 3',6'-isoLD1 distribution in cultured cell lines and derived xenografts of primary tumors of the human central nervous system and of embryonal or neuroectodermal tumor derivation was determined. Six of 29 cell lines expressed 3'-isoLM1: 2/16 gliomas, 3/3 teratomas, 1/1 pancreatic adenocarcinoma. No cell line expressed detectable 3',6'-isoLD1 by immunostain analysis of ganglioside extracts. The 3'-iso-LM1-positive cell lines expressed it in xenograft form; in five xenografts, the corresponding cell lines of which were 3'-isoLM1-negative, it was a proportion of the monosialoganglioside fraction. 3',6'-isoLD1 was detected in two xenografts, D-54 MG (glioma) and PA-1 (teratoma). The demonstration of 3'-isoLM1 in gliomas in in vivo forms and the relatively infrequent expression by derived cultured cells suggest that ganglioside expression is modified by environmental forces. Expression of 3'-isoLM1 and 3',6'-isoLD1 in fetal and neonatal brain, in intense reactive astrocytosis such as polyunsaturated fatty acid lipidosis, and in primary neoplasms of the central nervous system suggests their role in cell-cell attachment during development, migration, and neoplastic transformation.
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PMID:Occurrence of lacto series gangliosides 3'-isoLM1 and 3',6'-isoLD1 in human gliomas in vitro and in vivo. 174 82

Bilateral acoustic neurofibromatosis (neurofibromatosis 2, NF2) accounts for less than 10% of all cases of neurofibromatosis and manifests itself with bilateral acoustic schwannomas, multiple schwannomas of spinal nerve roots, meningiomas, glial tumors and hamartomatous CNS lesions. We have observed dysplastic foci of immature neuroectodermal cells in the cerebral cortex and basal ganglia of six patients afflicted with neurofibromatosis 2, ranging from occasional clusters of immature, dysplastic cells to numerous, confluent lesions. These cells, although often polymorphic and multinuclear did not show mitotic activity or a tendency for neoplastic transformation. To determine the histogenesis of these foci, extensive immunocytochemical reactions were carried out with antibodies to a variety of glial, neuronal and non-neural cell lineages. With the exception of S-100 protein, no immunoreactivity was detectable. S-100 was consistently expressed in these foci, irrespective of their size, location, and degree of polymorphism. On the basis of cytological appearance, distribution and immunoreactivity we tentatively designate these foci as glial micro-hamartomas. Although we did not systematically analyze the CNS of patients with von Recklinghausen neurofibromatosis (neurofibromatosis 1, NF1), the present study strongly suggests that these micro-hamartomas constitute a morphological hallmark of bilateral acoustic neurofibromatosis (NF2).
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PMID:Distribution and immunoreactivity of cerebral micro-hamartomas in bilateral acoustic neurofibromatosis (neurofibromatosis 2). 259 63

This is an autopsy case report of a 76 year old woman with multifocal glioblastoma multiforme. CT scan revealed three separate mass lesions in the left temporal lobe, left parietal lobe and right fronto-parietal lobes. CT-guided needle biopsy of the right fronto-parietal mass revealed glioblastoma multiforme. At autopsy, serial horizontal sections of the brain confirmed the CT scan findings and demonstrated extension of the tumor in the left parietal lobe to the subarachnoid space. The lesion in the right fronto-parietal region infiltrated a large area and was not demarcated. Microscopic examination of all three lesions revealed glioblastoma multiforme. The left temporal lobe tumor consisted of gemistocytic astrocytes predominantly. Reaction of the tumor to glial fibrillary acid protein (GFAP) antibody ranged from markedly positive in the gemistocytic astrocytes to negative in the anaplastic cells. The reported incidence of multifocal glioma is about 2-10%. The main pathophysiologic mechanisms invoked for this phenomenon are simultaneous neoplastic transformation and seeding from one tumor. The pathophysiology of this particular case is discussed in reference to the differences in the histopathology of the 3 separate foci of glioblastoma multiforme.
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PMID:[Multifocal glioma of the brain--an autopsy case]. 300 94

The vulnerability of neuroepithelial cells in the central nervous system (CNS) to neoplastic transformation results from the interaction of several factors: the existence of a reserve population of stem cells, the capability of differentiated cells to reenter the kinetic cycle, the number of replicating cells at risk at a particular time, the length of time during which a particular cell population remains in the cycle, the state of differentiation and the further differentiation potential of that population, and the steps of differentiation that are achieved in successive cell generations. This concept explains many aspects of CNS tumor incidence and the relationship of central neuroepithelial embryonal tumors to tumors of adult cell type. The incidence of different types of central neuroepithelial tumors can be correlated with the width of the window of neoplastic vulnerability. Examples illustrating the existence of only a narrow window include such rare tumors as medulloepitheliomas, cerebral neuroblastomas, gangliogliomas and ependymoblastomas. By contrast, cerebellar medulloblastomas, astrocytomas, mixed astrocytomas and oligodendrogliomas, and glioblastomas exemplify instances in which a relatively wider window of vulnerability exists in the light of cellular neuro-ontogeny and of the capacity of glial cells for postnatal replication. The relationship that may occasionally be established between the development of a glioma and the production of cellular gliosis such as may follow brain injury or accompany multiple sclerosis can also be viewed in the light of that concept. Increasing awareness is needed concerning the development of postradiation gliomas, in particular after the apparently successful treatment of acute lymphocytic leukemia.
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PMID:The correlation of neoplastic vulnerability with central neuroepithelial cytogeny and glioma differentiation. 303 35

Chronic myelogenous leukemia (CML) is an example of a "well-differentiated" neoplasm that develops following neoplastic transformation of a precursor cell. The biology of astrocytic neoplasms can be interpreted in light of concepts that have emerged from studies of the myeloproliferative disorders. Astrocytomas may arise from a pluripotential precursor cell whose progeny, although transformed, retain the ability to differentiate, and do so along astrocytic lines. The result is a neoplasm composed of "mature" tumor cells, similar one to another, and resembling normal astrocytes. Malignant change, like blast crisis in CML, then occurs as a consequence of further molecular genetic events leading to accelerated growth and maturation arrest in a previously differentiating neoplastic cell. This hypothesis challenges the conventional view that astrocytomas arise from astrocytes and that malignant change occurs as a result of dedifferentiation. Extensions of this hypothesis may be relevant to the biology of other glial tumors.
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PMID:The biology of astrocytoma: lessons learned from chronic myelogenous leukemia--hypothesis. 347 24


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