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)

Our studies demonstrate that rat anterior pituitary cells (GH3) are capable of synthesizing and secreting tissue kallikrein together with prolactin and growth hormone. The secretion of prolactin and growth hormone in GH3 cells was measured by two newly developed sensitive radioimmunoassays (RIA), using the polyethylene glycol separation technique. In the direct radioimmunoassay for rat tissue kallikrein, using a polyclonal antiserum which recognizes both active and prokallikrein, the GH3 kallikrein displays parallelism with standard curves of rat urinary kallikrein. The production of immunoreactive kallikrein, prolactin, and growth hormone is time-dependent, and the levels after a 72 h incubation in serum-free media are approximately 12.2 +/- 4.4 ng, 272.2 +/- 33.0 ng, and 475.6 +/- 4.8 ng per 10(6) cells per ml (mean +/- SD, n = 3), respectively. In Western blot analyses, a specific monoclonal antibody to tissue kallikrein (V4D11) identifies GH3-secreted kallikrein as a approximately 39,000 Da protein, slightly larger than approximately 38,000 Da kallikreins of submandibular gland, mouse anterior pituitary cells (AtT 20) or rodent neuroblastoma X glioma hybrid cells (NG108). Kallikrein mRNA in GH3 cells was identified in Northern blot analyses, using a tissue kallikrein cDNA probe. In a RIA using a kallikrein monoclonal antibody (V1C3) recognizing only active kallikrein, kallikrein could not be detected in the media incubated up to 48 h with GH3 cells. However, after trypsin treatment, a time-dependent increase of immunoreactive kallikrein (using monoclonal antibody V1C3), Tos-Arg-OMe esterase, and kinin-releasing activities can be measured in the conditioned media. The activated esterase activity was inhibited by aprotinin and by affinity-purified kallikrein monoclonal antibody (V4D11) in a dose-dependent manner. The data indicated that rat anterior pituitary GH3 cells secrete latent tissue kallikrein, which can be converted to active kallikrein by trypsin. These hormonally responsive cells co-synthesize kallikrein with prolactin and growth hormone and provide a model system for studying the regulation of kallikrein gene expression.
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PMID:Identification of latent tissue kallikrein, prolactin and growth hormone secretion in GH3 pituitary cells using modified radioimmunoassays. 336 Feb 6

The study of the autologous immune response to cancer avoids the difficulties encountered in the use of xenoantisera and may identify antigens of physiological relevance. However, the low titer and incidence of autologous antibody to melanoma have hampered further evaluation. By utilizing acid dissociation and ultrafiltration of serum, we have been able to augment the detectable autologous immune response to melanoma in the majority of patients studied. In autologous system Y-Mel 84:420, serum S150 demonstrated a rise in titer from 1:32 in native sera to 1:262,044 after dissociation. The antigen detected by S150 was found to be broadly represented on melanoma, glioma, renal cell carcinoma, neuroblastoma, and head and neck carcinoma cell lines. It did not react with bladder or colon carcinoma, fetal fibroblasts, pooled platelets, lymphocytes and red blood cells, or autologous cultured lymphocytes. Using polyacrylamide gel electrophoresis, S150 detects a 66,000-mol wt antigen in spent tissue culture media and serum ultrafiltrate. In cell lysate two bands between 20,000 and 30,000 mol wt are detected by S150. The 66,000-mol wt antigen is sensitive to trypsin digestion and but is resistant to pepsin and heat inactivation. Exposure of spent media to trypsin results in the development of a 24,000-mol wt band that appears to correspond to the antigen detected in the cell lysate. The difference between the antigens detected in the cell lysate as compared with spent media and serum ultrafiltrate may be due to degradation during cell lysis. We conclude that melanoma-associated antigens are present in the serum of patients with melanoma and are shed or secreted by their tumor cells.
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PMID:Isolation and partial characterization of melanoma-associated antigens identified by autologous antibody. 338 49

The killing of Fischer rat 9L glioma in vitro by lymphokine-activated killer (LAK) cells was studied. LAK cells generated by culturing Fischer spleen cells with recombinant interleukin 2 markedly lysed glioma cells but did not kill syngeneic normal brain tissue in a chromium release microcytotoxicity assay. Susceptibility of glioma to lysis by LAK cells was markedly diminished by pretreating the glioma cells with trypsin or chymotrypsin but was unaffected by pretreatment with neuraminidase, glycosidases, or sodium periodate. These results suggest that LAK cell killing of glioma is probably tumor-selective and that a crucial cell surface determinant on glioma cells responsible for its tumor-selective lysis by LAK is a protein sensitive to trypsin and chymotrypsin.
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PMID:Lymphokine activated killer (LAK) cell-mediated lysis of murine glioma: trypsin-chymotrypsin-sensitive glioma protein is responsible for tumor-selective recognition by LAK cells. 348 96

Methods are described to study cell surface and cytoplasmic antigens of cultured human glioma, fetal brain cells and fibroblasts using flow cytometry. This required harvesting the cultured cells with Versene or mild trypsin treatment and fixation in 4% paraformaldehyde prior to staining for glial fibrillary acidic protein (GFAP) and fibronectin using indirect immunofluorescence. At passage 10, 38% of fetal brain cells [CHII] were GFAP-positive but at passage 14 only 3.5% expressed GFAP. Two glioblastomas and an anaplastic astrocytoma had 38.8%, 6.7% and 81.3% GFAP-positive cells, respectively. Of the 10(4) cells studied, 91.6%, 79.1% and 40.8% were fibronectin-positive for glioblastoma multiforme [12-18], oligodendroglioma [12-10] and fetal brain [CHII] cells, respectively. Two fibroblast lines had 33.5% and 43.1% of the cells expressing fibronectin. The validity of these results was confirmed by staining for GFAP and fibronectin using peroxidase-antiperoxidase and immunofluorescence microscopy. Using low angle forward light scatter to estimate cell size and gating techniques it was found that GFAP-positive CHII and anaplastic astrocytoma cells were generally larger than GFAP-negative cells of the same type. No correlation between cell size and fibronectin expression was found for glioblastoma [12-18] cells. These results demonstrate the validity of the described methods and illustrate some specific applications and the potential value of flow cytometry to neurooncology.
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PMID:Application of flow cytometry to analyses of cultured human glioma and fetal brain cells. 388 48

Using three lines of human normal glial cells and four established lines of human malignant glioma cells we have studied cell spreading following seeding onto glass and plastic substrata. The cells were detached with EDTA and trypsin, suspended in EMEM with 10% calf serum and studied with time-lapse, phase-contrast cinematography in suspension and during attachment and spreading. Cells were fixed and prepared for light microscopy while in suspension and during the spreading process. They were also prepared for scanning and transmission electron microscopy at different times during spreading. The projected areas of stained cells, in suspension and at different stages of spreading, were measured morphometrically and the results compared statistically. The glial cells in suspension were often found to retain somewhat their shape from the previous monolayer. They spread radially outwards with even lamellar cytoplasm and peripheral ruffling, as a group more quickly than the malignant glioma cells. They also became polarized and started to translocate in a shorter time. The glioma cells were spherical in suspension and characterized by pronounced blebbing of the cell surface. Blebbing continued during spreading and was finally replaced by ruffling at the edge. The cells spread like the glial cells radially outwards but the lamellar cytoplasm was occasionally somewhat irregular. Cells from the glioma lines spread as groups slower than the glial cells but with individual rates for the different lines. One of the glioma lines appeared to spread more thinly than the glial cells. Cells which sedimented on top of other cells could not spread. Aggregations of cells spread and became polarized more quickly than single cells in all cases.
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PMID:The spreading of human normal glial and malignant glioma cells in culture. Studies on standard culture conditions. 390 65

Culture medium conditioned over C6 glioma cells (GCM) contains factors which induce neurite outgrowth from clonal rat pheochromocytoma (PC12) cells. The effects of GCM on the cell-substratum adhesion of PC12 cells, which is an early event required for the neurite outgrowth, were investigated. The results obtained are as follows. Addition of GCM promoted the adhesion of PC12 cells specifically to collagen-coated tissue culture dish. The GCM-promoted adhesion of PC12 cells was prevented by the treatment of the cells with cytochalasin B, concanavalin A and glycosidase mixture suggesting the contribution of microfilaments and cell surface carbohydrates in the cell adhesion. GCM did not increase significantly the intracellular content of cAMP and the extent of cell adhesion promoted by cAMP or dibutyryl-cAMP was much less than that by GCM. Two active factors contained in GCM were separated by either gel filtration or chromatofocusing using the cell adhesion assay as an index. The first factor with an apparent mol. wt. around 40,000 had the abilities to induce the neurite outgrowth and to enhance the choline acetyltransferase activity in addition to the ability to promote the adhesion of PC12 cells. The second factor with an apparent mol. wt. around 10,000 was devoid of the ability to induce the neurite outgrowth, but had the abilities to enhance the choline acetyltransferase activity and to promote the adhesion of PC12 cells. Both factors were sensitive to trypsin digestion and relatively heat stable. The significance of these factors in the neuronal differentiation was discussed.
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PMID:Promotion of cell-substratum adhesion of clonal rat pheochromocytoma cells (PC12) by factors contained in glioma-conditioned medium (GCM): separation of two active factors contained in GCM. 394 4

A macromolecule has been partially purified which influences the choice of the neurotransmitter synthesized by sympathetic neurons. Previous studies showed that culture medium conditioned by incubation on certain types of non-neuronal cells increased [3H]acetylcholine synthesis and accumulation from [3H]choline in primary cultures of neurons dissociated from neonatal rat superior cervical ganglion and grown in the virtual absence of non-neuronal cells. A concomitant decrease of [3H]catecholamines production was observed (Patterson, P. H., and Chun, L. L. Y. (1977) Dev. Biol. 56, 263-280). The active cholinergic factor in conditioned medium from C6 glioma or primary rat heart cultures has been purified about 1500-fold by a sequence of ammonium sulfate precipitation, DEAE-, CM-cellulose, and Sephadex G-100 chromatography. The partially purified factor is active at 1 microgram of protein/ml of culture medium and is eluted from Sephadex columns as a single peak of apparent Mr = 40,000-45,000. This material is insensitive to 0.2 M 2-mercaptoethanol, but is inactivated by 1 mM Na periodate. Its activity is partially decreased by treatment with a protease from Streptomyces griseus but is unaffected by neuraminidase. Material purified through the ammonium sulfate, DEAE- and CM-cellulose steps contains large amounts of trypsin- and chymotrypsin-inhibiting activities.
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PMID:A diffusible factor responsible for the determination of cholinergic functions in cultured sympathetic neurons. Partial purification and characterization. 611 Jun 68

Cells of the homogeneous hybrid line neuroblastoma x glioma (NG108-15) have many neuronal properties. Immunocytochemical tests show that they contain both immunoreactive renin and angiotensin; direct radioimmunoassays show that they are positive for renin, angiotensin I, and angiotensin II; enzymatic assays show that they contain angiotensinogen and converting enzyme as well. The renin appears to be present in an enzymatically inactive form that can be activated by trypsin and then blocked by antiserum to purified mouse submaxillary renin. Renin concentration and activity are increased by enhancing cellular differentiation with dibutyryl cyclic adenosine monophosphate or by serum withdrawal. These findings demonstrate a complete renin-angiotensin system within these neuron-like cells, and suggest that activation of intracellular renin could generate angiotensin II.
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PMID:Renin and angiotensin: the complete system within the neuroblastoma x glioma cell. 627 92

Partially purified extracts from neuroblastoma X glioma hybrid cells 108CC15 inhibit, like opioids, the prostaglandin E1-evoked formation of cyclic AMP in a dose-dependent manner in the same hybrid cells. The inhibition is prevented by the opioid antagonist naloxone. In addition, the same extract competes with [3H]naloxone and [3H]Leu-enkephalin for binding to opioid receptors of hybrid cell membranes and to a specific antiserum, respectively. The opioid activity in the extracts is destroyed by carboxypeptidase A and leucine aminopeptidase, but not by trypsin. Further purification of the extracts by HPLC, TLC, or high-voltage paper electrophoresis reveals in each case two active fractions which behave like Met- and Leu-enkephalin. The Met-enkephalin-like, but not the Leu-enkephalin-like, fraction is inactivated by treatment with BrCN. Dimethylaminonaphtylsulfonyl (dansyl) derivatives of Met- and Leu-enkephalin correspond to [3H]dansyl derivatives of Met-like substances from hybrid cells. Three to four times as much Met-enkephalin-like as Leu-enkephalin-like material is present in the extract. The overall concentration of opioid peptides in the hybrid cells varies between 0.03 and 1.0 pmol Leu-enkephalin equivalents per mg protein. The amount of opioids in the hybrid cells is strongly dependent on the cell density. The findings suggest that neuroblastoma X glioma hybrid cells contain opioid peptides that are very similar, if not identical, to Met- and Leu-enkephalin. Opioid activity can also be detected in other neuronal cell lines and even in glioma cells.
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PMID:Neuroblastoma X glioma hybrid cells synthesize enkephalin-like opioid peptides. 628 22

The nature of the refractoriness of C6 rat glioma cells to herpes simplex virus type 2 (HSV-2) was examined. Infection of C6 cells with HSV-2 results in low virus yields, not exceeding the input virus. Although virus growth studies suggested a restricted cycle of virus replication, synthesis of HSV-2 DNA and HSV-2-specific antigens could not be detected. In addition, HSV-2 yields in C6 cells were unaffected by interferon, cycloheximide, tunicamycin, actinomycin D and cytosine arabinoside. However, trypsin, but not EDTA, treatment of infected C6 cells at 4 hours postinfection (p.i.) reduced maximal HSV-2 yields at 24 hours p.i. by 61 percent. These data: 1) indicate that HSV-2 fails to replicate in C6 cells and is prohibited from directing the synthesis of virus macromolecules; and 2) suggests that the increment of HSV-2 yields observed during the synthesis phase of the virus growth cycle represents re-envelopment and egress of a portion of the input virus.
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PMID:Abortive infection of neural cells by herpes simplex virus type 2. 629 39


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