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)

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

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

Diffusion-weighted magnetic resonance imaging was used for the description of experimental brain tumors in rat. To validate this approach, diffusion-weighted images (DWI) were compared with native T1- and T2-weighted images, and with T1-weighted images following contrast enhancement with the tumor-specific contrast agent manganese (III) tetraphenylporphine sulfonate (MnTPPS). Three tumor types were studied: F98 glioma, RN6 Schwannoma, and E376 neuroblastoma. On heavily diffusion-weighted images, all three tumor types as well as the peritumoral edema were clearly hypointense with respect to the intact brain tissue. T2-weighted images presented mainly peritumoral edema as hyperintense region. A clear demarcation of the tumor was possible only on T1-weighted images after contrast enhancement with MnTPPS. The difference in signal intensity between tumor and homotopic regions in the contralateral hemisphere was comparable in DWIs and in contrast-enhanced T1-weighted images. Spatial comparison of depicted lesion areas in all three imaging modalities indicated that hypointense region on DWI represents both tumor and edema but does not permit their spatial differentiation.
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PMID:Diffusion-weighted MR imaging of experimental brain tumors in rats. 760 Jan 72

Chromatin condensation during apoptosis induced by TGF beta 1 in T24 glioma and 476-16 trigeminal neurinoma (Schwannoma) cells was examined and compared with that occurring during mitosis. Apoptotic (round-up) cells were selectively detached from the culture surface by a mechanical shock. Their histones were analysed in comparison with those obtained from TGF beta 1-treated cells remaining attached to the culture surface, from control cells not treated with TGF beta 1 and from metaphase cells. While mitosis-specific hyperphosphorylation of histones H1 and phosphorylation of histone H3 was not observed in apoptotic cells, apoptotic chromatin lacked ubiquitinated histone H2A (histone uH2A) as did metaphase chromosomes. The cellular level of free ubiquitin and the overall pattern of ubiquitin-conjugated proteins were, however, found to remain unaltered in apoptotic cells, suggesting that the ubiquitin conjugating machinery for histone H2A may be specifically perturbed during the chromatin condensation occurring in apoptosis.
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PMID:Disappearance of ubiquitinated histone H2A during chromatin condensation in TGF beta 1-induced apoptosis. 776 93

All previous studies of the localization of utrophin (the dystrophin-related protein) in muscle and other tissues have been performed only with antibodies against the C-terminal region of the protein. Since several short forms of dystrophin, the apo-dystrophins, are produced from the 3' end of the dystrophin gene, there is a possibility that similar short forms of utrophin exist and that these could be responsible for some of the many different localizations of 'utrophin' in muscle. We have produced a new panel of 15 mAbs against the N-terminal region of utrophin and we have used it together with mAbs against the C-terminal region to show that full-length utrophin is present at neuromuscular junctions, in nerves, blood vessels and capillaries in normal muscle and in the sarcolemma of patients with muscular dystrophy and dermatomyositis. However, two of the 15 mAbs also recognised rat/mouse utrophin and both of these detected an additional 62 kDa protein on Western blots of rat C6 glioma cells. This potential 62 kDa 'apo-utrophin' was not detected in human cerebral cortex, in rat Schwannoma cells nor in any of the non-nerve cells and tissues tested.
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PMID:Full-length and short forms of utrophin, the dystrophin-related protein. 784 13

Transforming growth factor beta 1 (TGF beta 1) inhibits cell proliferation in T24 glioma and 476-16 trigeminal neurinoma (Schwannoma) cells. In both cell types, the inhibition of cell proliferation is followed by cell rounding and detachment as well as internucleosomal DNA fragmentation, nuclear condensation and cell shrinkage, cellular changes that are characteristic for apoptosis. While the induction of apoptosis is closely coupled with the inhibition of cell proliferation in these tumor cells, the mode of apoptosis appears to differ between the two cell types. In 476-16 cells whose proliferation is highly susceptible to TGF beta 1, apoptosis occurs primarily after growth arrest at the G1 phase. Apoptotic cell death of 476-16 cells pretreated with TGF beta 1 is stimulated by serum deprivation, and it is inhibited by mitogenic growth factors such as insulin and platelet-derived growth factors. In T24 cells whose DNA replication is inhibited only moderately by TGF beta 1, apoptosis occurs in the presence of TGF beta 1 during the final cell division cycle when cells undergo density-induced growth arrest. While staurosporine accelerates TGF beta 1-induced apoptosis in both 476-16 and T24 cells, 12-O-tetradecanoylphorbol 13-acetate inhibits TGF beta 1-induced apoptosis of 476-16 cells but stimulates that of T24 cells. The present results suggest that TGF beta 1 may potentially be utilized for the management of neurogenic tumors of glial and Schwann cell origin.
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PMID:Induction of apoptosis by transforming growth factor beta 1 in glioma and trigeminal neurinoma cells. 787 62

The detection of brain tumors using standard techniques of qualitative, relaxation-weighted magnetic resonance imaging (MRI) requires the application of contrast agents. We investigated whether or not it is possible to use diffusion-weighted MRI to localize tumors without contrast enhancement. Three different experimental rat brain tumors were studied: F98 glioma, RN6 Schwannoma and E376 neuroblastoma. We found a marked hypointensity in the region of the tumor and edema in heavily diffusion-weighted images, which corresponded well with the histological presentation. Quantitative maps of the apparent diffusion coefficient (ADC) allowed a better localization of the tumor than that obtained by regional presentation of T2 times, particularly under conditions in which peritumoral edema was absent. The ADC differences of the three tumor types were statistically not significant. Based upon regions-of-interest evaluations, tumor could be distinguished from peritumoral edema and normal brain tissue. However, a sharp demarcation between tumor and peritumoral edema was not possible, and this is attributed to a similar enlargement of interstitial space. It was concluded that diffusion-weighted MRI possesses a high potential for the detection of brain tumors but does not allow precise demarcation of the tumor border.
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PMID:Quantitative diffusion MR imaging of cerebral tumor and edema. 797 85

The potential of quantitative parameter images of the relaxation times T1 and T2, the proton density rho and the apparent diffusion coefficient (ADC) to characterize three different experimental rat brain tumors (F98 glioma, RN6 Schwannoma, and E376 neuroblastoma) was studied. All parameter values, as determined in histologically confirmed regions of interest (ROI), were higher in edema than in tumor, which in turn were elevated with respect to normal brain. ROI values of ADC and T2 delivered statistically significant (P < 0.01) differentiation between tumor and edema. Multidimensional parameter combinations improved differentiation between different tissues. However, the three tumor types could not be differentiated. All parameter maps allowed the identification of the whole tumor-edema area. On T2 images, edema could be identified best, whereas the tumor itself was hardly visualized. In many cases, tumor presentation using T1 maps corresponded best with histology, nevertheless suffering from a poor tumor-edema differentiation.
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PMID:High resolution quantitative relaxation and diffusion MRI of three different experimental brain tumors in rat. 859 10

Schwannoma-derived growth factor (SDGF) is a member of the epidermal growth factor (EGF) family, having mitogenic activity on rat astrocytes, fibroblasts and Schwann cells. The SDGF gene is significantly expressed in the newborn rat lung and in the adult rat sciatic nerve. However, except for one rat schwannoma cell line, from which SDGF and its cDNA were isolated, nothing is known about SDGF expression in established tumor cell lines. We examined the expression level of the SDGF gene in a variety of rat tumor cell lines by Northern blotting and found that it was increased in 11 of 25 established lines. The most abundant SDGF mRNA, which was about 50-fold higher than in the newborn rat lung, was expressed in rat liver adenoma dRLa74 cells. In rat glioma cell lines, such as C6, 9L and T9, and in the rat hepatoma dRLh84 and H411E cells, the SDGF expression level was about 10-fold higher than in the newborn rat lung. In 8 of 13 cell lines expressing SDGF mRNA, the EGF receptor (EGFR) gene, the product of which is regarded as a functional receptor of SDGF, was co-expressed. In addition, transfected gene-dependent anti-sense SDGF RNA expression under the control of the human metallothionein promoter significantly suppressed the in vitro growth as well as in vivo tumorigenicity of 9L glioma cells. Our results suggest that SDGF acts as an autocrine growth factor in the development and growth of rat tumors such as gliomas.
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PMID:Increased expression of schwannoma-derived growth factor (SDGF) mRNA in rat tumor cells: involvement of SDGF in the growth promotion of rat gliomas. 862 Dec 57


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