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

Spleen cells from BDIX-rats bearing either GVlAl-tumor (a syngeneic mixed glioma) or NVlAc-tumor (a cloned syngeneic neurinoma of the peripheral nervous system) were cytotoxic to both tumor cells in vitro. However, the tumors displayed individually distinct antigenic specificities by in vivo rejection tests. Their in vitro cross-reactivity disappeared when a particular subpopulation of the spleen cells was used. The procedure of lymphocyte purification included three consecutive steps: treatment with carbonyl iron and magnetism, passage through a nylon wool column, and finally removal of complement receptor-bearing cells present in the colum-excluded population. Cross-reactivity between the syngeneic tumors persisted after the first two steps of lymphocyte purification. In contrast, specific cytotoxic reactions were observed against each individual tumor subsequent to the removal of the remaining C3 receptor-positive but surface Ig-negative cells. While killer cells were present in normal spleen-cell populations, these were almost completely eliminated by passage through the nylon wool column.
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PMID:Spleen-cell reactivity against transplanted neurogenic rat tumors induced by ethylnitrosourea: uncovering of tumor specificity after removal of complement-receptor-bearing lymphocytes. 5 Feb 96

The concurrent daily intragastric administration of ethylurea at two dose levels (50 mg/kg and 100 mg/kg bodyweight) together with one dose level of sodium nitrite (50 mg/kg bodyweight) by a stomach tube to pregnant BD IX rats from day 15 to day 22 of gestation resulted in the induction of neurogenic tumors in all offspring. Since both ENU-precursors alone do not produce neurogenic tumors, these results are evidence of ENU formation from its precursors under the influence of gastric juice. Differences in the survival time and the incidence of tumors at both dose levels were not significant. The amount of ethylnitrosourea synthesized in the animals was very close at both dose levels, and was dependent on the amount of sodium nitrite applied. The experimental results are consistent with the conclusion, that the rat fetuses had been exposed to a total amount of about 60 mg/kg ethylnitrosourea. Neurogenic tumors dominated with 98% incidence over the non-neurogenic. The incidence of neurogenic tumors per rat was high (6.0 for Group I and 6.7 for Group II). Neurogenic tumors were equally distributed among the central and peripheral nervous systems. The neurogenic tumors induced with the precursors of ethylnitrosourea were morphologically similar in all aspects to those induced with the carcinogen itself and could be classified as oligodendroglioma, astrocytoma, mixed glioma, anaplastic glioma, glioependymoma, ependymoma, and neurinoma. Three unusual tumors were found: one early anaplastic "septum ependymoma" in the dorsal column of the spinal cord, and two special mixed tumors of the cranial nerves, i.e. a neurinoma with portions of an oligodendroglioma and a neurinoma with parts of an invasive ependymoma.
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PMID:Transplacental induction of neurogenic tumors in BD IX rats by intragastric administration of ethylnitrosourea precursors. 12 44

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

Addition of 1 micronM 1-norepinephrine to cultures of C6TK- rat glioma cells caused a 2-fold increase in specific activity of the glial-specific enzyme 2':3'-cyclic nucleotide 3'-phosphohydrolase (nucleoside-2':3'-cyclic-phosphate 3'-nucleotidohydrolase, EC 3.1.4.16). Specific activity could also be stimulated by analogues of 3':5'-cyclic AMP, and the effect of norepinephrine could be blocked by beta-adrenergic receptor antagonists but not by alpha-adrenergic antagonists. Norepinephrine or cyclic AMP analogues also increased the specific activity of this enzyme in other clones of glioma and Schwannoma cells and in glioma X neuroblastoma cell hybrids. These results show that the stimulatory effect of norepinephrine on cyclic AMP concentrations in glioma cells leads ultimately to a stimulation of glial-specific cell funtion.
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PMID:Norepinephrine induces glial-specific enzyme activity in cultured plasma glioma cells. 20 Sep 19

Several neural cell lines were examined for their ability to synthesize sulfatide and 2',3'-cyclic nucleotide phosphohydrolase, biochemical components characteristic of myelin. The mouse glioma G26 and the rat schwannoma TRM6B actively produced sulfatide, while the rat glioma C6 was inactive, supporting the probable oligodendroglial origin of the G26. In contrast, the C6 cell line had a high level of 2'-3'-cyclic nucleotide phosphohydrolase activity, while TRM6B showed 30% and the G26 75% lower activities. Thus, these two activities appear to be independently regulated.
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PMID:Sulfatide synthesis by neural cell lines. 23 75

The composition of the free amino acid pools in various brain tumors and in normal brains obtained at surgery or at autopsy is determined with an automatic amino acid analyzer and the results statistically evaluated. The tumors have lower ratios of GABA in the pools than the normal brain; tumors with higher GABA ratios are found in those which are in close contact with and have an invasive nature to brain tissue. In gliomas, the more malignant a tumor becomes, the more different the composition in that tumor is from that in normal brain tissue. But conversely, the ratio of GABA is highest in glioblastoma. The composition of the pool in oligodendroglioma is not significantly different from that in the normal brain. Metastatic brain tumors show the highest ratios of phenylalanine, tyrosine and methionine in the pool among the tumors and the normal brain. From the viewpoint of the composition of the free amino acid pools, like from that of the histological aspects, brain tumors seem to be classified into four groups: glioma, neurinoma, meningioma and metastatic tumors.
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PMID:Composition of free amino acids in brain tumors. 54 90

The chromosomes in 15 cell lines derived from separate tumors induced in rats by ethylnitrosourea (ENU) are described. Thirteen lines were neural (glioma or schwannoma) in origin and type. In 12 of these lines, excess chromosome no. 4 could be demonstrated by Giemsa banding. One to three extra no. 4 chromosomes were seen as numerical or structural abnormalities. Also noted were other changes that were not consistent among lines. The 12 lines produced tumors in newborn rats. The 13th neurogenic line lacked excess chromosome no. 4 and did not produce tumors. The remaining 2 lines were nonneurogenic and lacked excess chromosome no. 4 but produced tumors. Control studies included chromosome analyses of bone marrow preparations from ENU-treated rats with tumors, cell lines from brains of normal rat embryos, and 2 established nonneurogenic rat tumor lines. No excess chromosome no. 4 was seen. These results suggest that nondisjunction and/or rearrangement of chromosome no. 4 is associated with the oncogenic process in neurogenic tumors induced.
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PMID:Excess chromosome no. 4 in ethylnitrosourea-induced neurogenic tumor lines of the rat. 56 44

We used a new immunocytoadhesion method to test 15 different tumors of the human nervous system to see whether medulloblastomas share tumor-associated surface antigens (TSA) with other tumors. Antisera against medulloblastoma cells were raised in rabbits. One antiserum was adsorbed extensively with tonsil and adenoid cells and with cerebral tissues. Freshly isolated cells from 15 different tumors were first sensitized with the adsorbed antiserum and then rosetted with erythrocytes coated with purified antibody to rabbit immunoglobulin. We found that the antimedulloblastoma antiserum detected TSA on the immunizing medulloblastoma cells and on cells from 2 other medulloblastomas, but apparently not on cells from other tumors (astrocytomas, glioblastomas, neurinoma, meningiomas and craniopharyngioma). In addition, the antiserum probably detected the medulloblastoma TSA on some other tumors (oligodendroglioma, ependymoma and malignant glioma of mixed type).
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PMID:Comparison of tumor-associated surface antigens on cells from medulloblastomas and from other neoplasms of the human nervous system. 56 78

Experimental cerebral tumors have been induced by transplacental ENU. A systematic diachronic study of the brains has been performed starting from the 15th day of extrauterine life. The tumoral lesions firstly appear as "early stage proliferations" or oligodendroglial foci and develop as glial micro- and macrotumors or as isomorphic and polymorphic oligodendrogliomas respectively. Neurinomas appear later than glial tumors. The duration of the different lesions is sketched out. The usefulness of the model for chemotherapy studies is discussed.
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PMID:Cerebral tumors induced by transplacental ENU: study of the different tumoral stages, particularly of early proliferations. 63 34

The surface structure of a series of malignant neurogenic rat cell lines in culture has been investigated by scanning electron microscopy. Neoplastic transformation was induced by a single transplacental administration of the carcinogen ethylnitrosourea (ENU) to BD-IX rats on the 18th day of gestation. The malignant cell lines were established either by explantation into culture of cells from solid gliomas or neurinomas developed in the offspring, or by transfer of fetal brain cells to culture where they subsequently underwent malignant transformation. A high degree of surface activity was observed, as evidenced by microvilli, filopodia, ruffling membranes and zeiotic blebs. Surface activity was highest in cell cultures giving rise to glioma-like tumours upon re-implantation into syngeneic hosts, and low in those giving rise to neurinoma-like tumours, with one exception. The lowest surface activity was seen in a cell line which was not tumourigenic. High surface activity was mostly correlated with a high degree of aneuploidy. No correlation was apparent with other properties of the neoplastic cell lines, e.g., stem line ploidy and population doubling time in cell culture.
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PMID:Scanning electron microscopy of neoplastic neurogenic rat cell lines in culture. 69 13


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