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)

Isoenzyme spectrum and total activity of arginase were studied in rat brain during growth of transplanted neurinoma and glioma as well as in malignant tissues of human brain. After transplantation of the tumors two peaks of arginase activation were observed within 2-4 days in rat brain tissues and within 16 days in tumoral tissue. Positively charged isoenzyme I of arginase was mainly activated but activity of neutral isoenzyme II was unaltered or slightly decreased. In human brain tumors activity of isoenzyme I was also prevailed, while activity of isoenzyme II was increased in some cases. Regulation of the arginase activity appears to occur by a complex mechanism and the enzyme plays a key role in development of nervous tissue neoplasms.
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PMID:[Comparative study of the activity of arginase isoenzymes in brain tumors of humans and experimental animals]. 381 Dec 80

Adrenal chromaffin cells from early postnatal rats maintained in culture have previously been shown to grow neuritic processes and survive better in the presence of nerve growth factor (NGF). In the present study we have quantitated the effects on chromaffin cell (postnatal day (D) 8) survival and neurite outgrowth of: NGF, ciliary neuronotrophic factor (CNTF), activities contained in various types of conditioned media (CM), and various substrata (laminin, fibronectin and polyornithine-binding neurite-promoting factor from RN 22 Schwannoma cells - PNPF). At saturating concentrations CNTF (50 ng/ml) and C6 glioma cell CM, (50-fold concentrated) supported survival over the 4-day culture period of all the chromaffin cells present in culture 2 h after seeding. NGF (50 ng/ml) and the non-concentrated CMs from primary Schwann cell and astrocytes as well as Schwannoma and C6 glioma cell cultures, achieved the maintenance of only about half the number of cells above the baseline survival as compared to CNTF and the concentrated C6-CM. These results are compatible with two subsets of D8 chromaffin cells, one only supported by CNTF and the concentrated CM and the other supported by either NGF or CNTF. Either NGF or CNTF elicited neurite outgrowth from 15-20% of the surviving cells. Combination of maximal doses of NGF and CNTF caused a small increase in neurite recruitment beyond that elicited by either factor alone. Low doses of CNTF added to the effect of NGF, shifting the NGF titration curve by about 4-fold. Neurite outgrowth was also induced by the concentrated, but not the unconcentrated C6-CM. Laminin, fibronectin and PNPF did not affect the fibronectin and PNPF did not affect the recruitment of neurites as compared to a polyornithine substratum unless the cultures were supplemented with a neuronotrophic factor and carried for 7 days. However, even before showing effects on neurite recruitment these substrata affected various neuritic performances, such as length, neurite numbers and endings per cell.
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PMID:Neuronotrophic and neurite-promoting factors: effects on early postnatal chromaffin cells from rat adrenal medulla. 398 81

The monoclonal antibody 217c, raised by Peng et al. [(1982) Science, Wash. 215, 1102-1104] in mice against the rat glioma cell line C6, can be used as a marker for normal Schwann cells. In mixed cultures of Schwann cells and fibroblasts from neonatal rat sciatic nerve, this monoclonal antibody, detected by indirect immunofluorescence, bound to the surface of cells with the same elongated morphology as those that express a previously described surface antigen, rat neural antigen-1 (Ran-1), defined by polyclonal mouse antisera. In these experiments Ran-1 and the antigenic determinant recognized by monoclonal 217c were both found on normal rat Schwann cells and on the rat glial tumor cell lines C6, 33B and 21A and the pheochromocytoma PC12. Neither anti-Ran-1 nor the monoclonal antibody bound to neurons, fibroblasts or glial cells in newborn rat cerebellum cultures, the rat muscle cell line L6, the transformed rat fibroblast cell line Rat 1, the rat brain tumor cell line B28 or the mouse Schwannoma cell line TR6B. Thus the monoclonal 217c behaved as if it were detecting Ran-1 by binding to normal rat Schwann cells and to those tumor cells that have this antigen. Our data show that this monoclonal antibody is a reliable and convenient marker for rat Schwann cells in culture.
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PMID:A monoclonal antibody equivalent to anti-rat neural antigen-1 as a marker for Schwann cells. 406 57

A serum-free defined medium has been formulated that supports proliferation and morphologic differentiation of U-251 MGsp human and C6-2BD rat glioma cells. This defined medium consists of a basal medium supplemented with transferrin, fibroblast growth factor, hydrocortisone, selenium, biotin, and fibronectin (G2 medium). When U-251 cells were plated in G2 medium on poly-D-lysine precoated dishes, their growth rate was 77% and final cell density was 82% of serum-grown counterparts. The growth rate of C6 cells in G2 medium was 67% compared to cells cultured in serum supplemented medium. Although G2 medium supported the growth of human and rat glioma cells, LA-N-1 human neuroblastoma and WI-38 human fibroblast cells showed no increase in cell number when grown in G2 medium compared to basal medium. A similar formulation (G3 medium), lacking fibroblast growth factor and hydrocortisone, supported the proliferation of RN-22 rat schwannoma cells. Morphologic differences were observed between cells grown in the presence of serum and in defined media. All three glial cell lines changed from a flattened shape in serum supplemented medium to a more spherical appearance in defined medium. In addition, both U-251 and C6 cells developed numerous processes, some reaching several cell diameters in length. These defined media will facilitate studies of the growth and differentiation of glial-derived cells.
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PMID:Proliferation of glial-derived cells in defined media. 621 93

1. After s.c. and intracerebral (i.c.) inoculation, 4 neurogenic tumors of the rat (3 malignant neurinomas, 1 polymorphcellular glioma) revealed an altogether weak response towards a monotherapy with 1,3-bis(2-chloroethyl)-1-nitrosourea(BCNU), 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU), 1-(2-chloroethyl)-3-(4-Methylcyclohexyl)-1-nitro sourea (MeCCNU), 1-(2-hydroxyethyl)-3-(2-chloroethyl)-3-nitrosourea (OH-ethyl-CCNU), 2-[3-(2-chloroethyl)-3-nitrosoureidol]-D-glucopyranose (chlorozotocin), 5-(3,3-dimethyl-1-triazeno)-imidazol-4-carboxamide (DTIC). Cyclophosphamide (CPA) which was investigated for comparison showed the greatest therapeutic activity; in an equitoxic dosage (less than or equal to LD10), in all 4 s.c. tumors, partial or complete regression were effected only by CPA. 2. If the passage number increases, the response of transplanted neurogenic rat tumors to monochemotherapy can both increase and decrease. 3. In the monotherapy of 3 malignant neurinomas we were unable, on the whole, to observe a higher sensitivity after s.c. inoculation as compared with an i.c. inoculation of the tumor, despite a varying effectiveness of the single substances. 4. In the monotherapy of the polymorphcellular glioma a better response of the i.c. inoculated tumor was recognizable compared to the s.c. inoculated tumor. 5. A combination chemotherapy of a malignant neurinoma after s.c. and i.c. inoculation with vincristine, CPA, OH-ethyl-CNU and MeCcNU yielded a significant increase in life-span of animals with i.c. tumor, whereas s.c. tumors showed no significant growth inhibition. y. Transplanted neurogenic tumors of the rat could serve at less sensitive models for the investigation of new nitrosoureas.
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PMID:[Chemotherapy of transplanted neurogenic tumors in the rat (author's transl)]. 626 27

The effects of mitogenic lectins Phytohemagglutinin (PHA), and Concanavalin A (Con A) on the growth rate of cells derived from glial tumors (astrocytoma, ependymoma, glioblastoma, medulloblastoma, and C6 rat glioma), neural crest tumors (neuroblastoma and schwannoma), and meningiomas were studied. The cell lines were of human and animal origin. The specificity of lectin binding to mitogenic receptors was evaluated using complementary monosaccharides. In all glial- and some neural-crest tumor-derived cell lines, there was a lectin concentration-dependent and cell density-dependent, biphasic growth rate response with stimulation at low and inhibition at high lectin concentrations. This response did not depend on the type of glial tumor, species of origin, or passage level in vitro. Although, in meningioma-derived cell lines, lectins did not induce a growth rate response, they caused morphological changes ("whorling"). Lectin stimulation in glial tumor-derived cell lines resembles that occurring in peripheral blood lymphocytes. Lectin-induced mitogenesis may lay the groundwork for the establishment of a model of glial cell proliferation, and that permits the evaluation of cell surface effects, intracellular mechanisms, and epigenetic factors in studies of tumors, neural development, and neuroimmunology.
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PMID:Mitogenic lectin receptors of nervous system tumors. Study of gliomas, neural crest tumors, and meningiomas in vitro using phytohemagglutinin and concanavalin A. 628 95

The effects of glia maturation factor (GMF) on cell proliferation and differentiation were investigated with 3 astroglioma cells (GE-12, C6, and GA-1), Schwannoma-like cells (354A), and mixed glioma cells (LRM-55). In the exponentially growing phase the growth rates of all glioma cells were enhanced by GMF regardless of the presence or absence of serum, but the factor failed to make the saturation density surpass the control level observed in the medium without GMF even in the chemically defined medium (N2 medium). GMF markedly lowered the saturation density of Schwannoma-like cells in N2 medium. Although GMF increased the intracellular content of S-100 protein 10-fold and 2',3'-cyclic nucleotide phosphohydrolase activity 1.5-fold in Schwannoma-like cells, GMF conversely decreased the S-100 contents and glycerol phosphate dehydrogenase activity in astroglioma cells. All the astroglioma cells secreted into the culture medium large quantities of a growth-promoting factor(s) which had similar chemical properties to those of GMF and stimulated the proliferation of normal glioblasts; but Schwannoma-like cells did not, although they produced a small amount of such a factor(s). These findings imply that astroglioma cells are deprived of the differentiation-promoting response to GMF while Schwannoma-like cells still preserve the response in addition to the proliferative response to GMF.
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PMID:The absence of differentiation-promoting response of astroglioma cells to glia maturation factor. 632 49

This review deals with steroid hormones and receptors in relation to the physiology and the pathology of the central nervous system (CNS) and meninges. In recent years experiments performed in animals showed that: 1) endogenous steroid hormones cross the blood brain barrier: 2) radiolabelled steroid hormones bind in specific areas of the CNS; 3) all five classes of steroid receptors, i.e. oestrogen, progesterone, androgen, glucocorticoid and mineralocorticoid receptors (OR, PR, AR, GR, MR), are present in brain tissues, especially in the hypothalamus and the limbic system; 4) the interaction of steroid hormones and specific receptors induces the synthesis of proteins in the CNS; 5) finally, in situ metabolism of steroid hormones has been evidenced by the presence of specific enzymes. A few studies in human brain tissues have shown the presence of GR and OR as well as enzymes involved in the metabolism of sex steroid hormones. In neurology, some epidemiological and clinical data suggest the implication of steroid hormones and receptors in human CNS: 1) the influence of oestrogens in tardive dyskinesia; 2) the relevance of hormonal changes in benign intracranial hypertension; 3) the usefulness of glucocorticoid therapy in many patients with intracranial tumors and/or edema. Due to feasibility, most researches have concerned tumors: meningioma, neurinoma and glioma. Firstly, a reappraisal of biochemical and histochemical technics used to detect and characterize the receptors in tumors is presented. Then results from the recent literature are reviewed. In meningioma, PR was found in 89 p. 100 (152/177) of the cases, usually at moderate to high levels (up to 33 000 fmol/gT). In addition, PR has been fully characterized from a biochemical point of view. Furthermore, it has been hypothesized that PR may be a marker of leptomeningeal cells since it was detected at high levels in well differentiated tumors provided they had no or few psammoma. This was further supported by the discovery of PR in normal leptomeninges in human adults. OR was detected in 48 p. 100 (87/177) of the meningioma, at low levels. This is in contrast with PR but the percentage of cases with OR raises to 70 p. 100 (42/60) if one considers only tumors assayed for both cytosolic and nuclear receptors. Therefore it has been suggested that OR had translocated into the nucleus, at least in some cases, and subsequently the hypothesis of functional OR in meningioma was raised. AR was also detected in meningioma. Furthermore AR levels were found to correlate well with PR levels.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Steroid receptors in the central nervous system. Implications in neurology]. 637 95

Neuronotrophic factors, a class of macromolecules thought to be present within the neuronal environment are required to support the survival in vitro of peripheral neurons. In the present study we have established bioassay culture systems suitable for the identification of similar agents for intrinsic neurons of the central nervous system. The striatum, hippocampus and septum of 18 day fetal rats were dissociated and plated in a serum-free medium on a neurite conducive substratum which allows an easy recognition of neurons under phase contrast microscopy. These cultures contain predominantly neurons as assessed by tetanus toxin labelling, a well recognized neuronal marker. Seeding the cell suspensions at decreasing densities yields after 24 h a density dependent survival of the neuronal population. Thus a low seeding density could be chosen where survival of these neurons required an exogenous source of trophic factors. Survival of central neurons was promoted by several conditioned media derived from rodent glial cell cultures, both primary (astroglia, Schwann) and clonal (C6 glioma, Schwannoma). Serial dilutions of these media allowed the titration of their respective neuronotrophic activities. In addition, conditioned media derived from the central neuronal cultures themselves, when seeded at a high density, were also able to support the survival of low density seeded central neurons.
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PMID:Use of central neuronal cultures for the detection of neuronotrophic agents. 637 2

An autopsy case of von Recklinghausen's disease (vRD) associated with malignant pheochromocytoma is reported. The patient is a 36-year-old Japanese male and diagnosed as vRD both clinically and pathologically. He died from right adrenal tumor with wide spread metastases to lungs and bone marrow. The tumors presented satisfactory histological features in favor of pheochromocytoma and neurosecretory granules were demonstrated in both primary and metastatic lesions ultrastructurally. Statistical study of 182, 673 autopsy cases from Annuals of Japanese Autopsy Cases was also done in order to investigate the relationship between vRD and associating tumors including benign and malignant pheochromocytoma. Cases with vRD showed significantly higher incidences of malignant Schwannoma, neurofibrosarcoma, intracranial glioma, and pheochromocytoma compared to that of non-vRD cases. Other malignancies revealed rather smaller incidences than non-vRD cases. These neurogenic tumors are to be principal life threatening problems in patients with vRD. Rare incidence of malignant pheochromocytoma in vRD is to become from low incidence of pheochromocytoma, though significantly greater than that of non-vRD cases.
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PMID:Von Recklinghausen's disease (neurofibromatosis) associated with malignant pheochromocytoma. 643 30


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