Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Small animal models such as the rat have serious limitations for multiple human scale instrumentation, surgical manipulations, and computerized tomographic (CT) evaluations, so that large animal models are required for the study using them. Although brain tumors induced with Rous sarcoma virus in neonatal beagle or adult monkey had been reported, these animals are very expensive ones for tumor research. A major drawback of virally induced brain tumor model is, moreover, the need for specialized viral facilities and safety precautions for laboratory personnel. In this paper, a cat glioma model implanted with C6 glioma cells derived from rats injected with N-nitrosomethylurea is reported. For an implantation dose of 5 x 10(5) cells/50 microliters, C6 glioma cells were suspended in modified Eagle medium supplemented with 10% fetal bovine serum and 0.5% agar. Twenty adult mongrel cats were injected with 5 x 10(5) C6 glioma cells intracerebrally. Implanted cats had brain tumors of about 10 mm in diameter with a yield of 80%. The mean survival was about 3 weeks after implantation. Tumors developed as spheroidal, hemorrhagic masses with central areas of necrosis and peripheral edema. They were located within the parenchyma of the implanted region. This tumor possessed many of the histological and radiological characteristics of human glioblastoma such as the following: Areas of hemorrhage and necrosis surrounded by pseudopallisading were observed within the tumor consisting of spindle-shaped cells with pleomorphic nuclei. A mass lesion with ring or garland-like enhancement surrounded by brain edema was shown on the CT scans.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Experimental brain tumor in adult mongrel cat]. 239 Mar 66

Monoclonal antibodies raised against B 16 melanoma cells in syngeneic mice were functionally screened for their ability to inhibit cell adhesion in tissue culture. Three of these antibodies (16/43, 16/77, 16/82), when preinjected into C57BL/6 mice, markedly reduced the number of experimental lung metastases produced by B 16 cells, possibly by interference with their adhesion to the lung endothelia. We now report that these monoclonal antibodies block in vitro attachment of the majority of human melanoma cell lines tested and also of carcinoma, neuroblastoma, and glioblastoma cells from both mice and humans but untransformed cell lines such as 3T3 mouse or MRC-5 human fibroblasts are not affected. The antibodies also react with mouse teratocarcinoma stem cells (F9, PCC4) but not with differentiated teratocarcinoma lines (PYS-2, 944). Furthermore, the antiadhesion activity of the antibodies could be quantitatively absorbed by intact human and mouse tumor cells but not by untransformed cells, suggesting that the corresponding antigens may represent tumor-associated cell surface components. Correspondingly, the antigens were found on simian virus 40-transformed 3T3 mouse fibroblasts and are expressed in a temperature-sensitive fashion in chicken fibroblasts transformed with a temperature-sensitive Rous sarcoma virus. On "immunoblots" of NaDodSO4-containing gels the three selected antibodies (16/43, 16/82, 19/1) were absorbed by antigens with molecular weights of 40,000 and 50,000.
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PMID:Monoclonal antibodies that prevent adhesion of B 16 melanoma cells and reduce metastases in mice: crossreaction with human tumor cells. 631 31

We have re-examined whether pp60c-src, the normal cellular homologue of the transforming protein of Rous sarcoma virus, is present in human T cells. By in vitro immune-complex kinase assay or Western blotting with the anti-pp60c-src mAbs 327 or GD11, pp60c-src was found to be present in lysates of T cell lines, including the Jurkat T cell line. The 327 and GD11 mAbs have been reported to be specific for pp60c-src and not to cross-react with other src family members or other kinases. Furthermore, the size of the pp60c-src bands present on Western blotting and in vitro kinase assay were clearly different from those of p56lck or p59fyn. In addition, pp60c-src is detected in the HTLV-I-derived T cell lines S1T and C8, which lack expression of p56lck and p59fyn. RNase protection assays confirmed that pp60c-src mRNA is present in Jurkat T cells. We also found pp60c-src protein to be constitutively present in freshly isolated thymocytes. In contrast, pp60c-src was absent, or present at extremely low levels, in normal, resting peripheral blood T lymphocytes, which is in agreement with previous findings. However, after stimulation of resting T cells with the mitogenic lectin PHA or with Ab to the TCR complex, pp60c-src expression is induced in both CD4+ and CD8+ T cell subsets, with peak expression detectable 12 to 24 h after T cell activation. The levels of pp60c-src are low in all T cells except Jurkat, where levels of pp60c-src are comparable to levels found in a glioblastoma cell line (T98G). Nevertheless, significant levels of pp60c-src kinase activity are readily detectable in thymocytes and activated normal T cells as well as in T cell lines. The finding that pp60c-src is inducible following activation through the TCR suggests that pp60c-src may play a specific role in the normal T cell activation pathway.
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PMID:pp60c-src expression is induced by activation of normal human T lymphocytes. 753 11

We describe the construction and characterization of retroviral vectors and packaging plasmids that produce helper-free retrovirus with titers of 1 X 10(6) to 5 X 10(6) within 48 h. These vectors contain the immediate early region of the human cytomegalovirus enhancer-promoter fused to the Moloney murine leukemia virus long terminal repeat at the TATA box in the 5' U3 region, yielding the pCL promoter. By selecting vectors designed to express genes from one of four promoters (dihydrofolate reductase, Rous sarcoma virus, long terminal repeat, or cytomegalovirus), the pCL system permits the investigator to control the level of gene expression in target cells over a 100-fold range, while maintaining uniformly high titers of virus from transiently transfected producer cells. The pCL packaging plasmids lack a packaging signal (delta-psi) and include an added safety modification that renders them self-inactivating through the deletion of the 3' U3 enhancer. Ecotropic, amphotropic (4070A), and amphotropic-mink cell focus-forming hybrid (10A1) envelope constructions have been prepared and tested, permitting flexible selection of vector pseudotype in accordance with experimental needs. Vector supernatants are free of helper virus and are of sufficiently high titer within 2 days of transient transfection in 293 cells to permit infection of more than 50% of randomly cycling target cells in culture. We demonstrated the efficacy of these vectors by using them to transfer three potent cell cycle control genes (the p16(INK4A), p53, and Rb1 genes) into human glioblastoma cells.
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PMID:The pCL vector system: rapid production of helper-free, high-titer, recombinant retroviruses. 876 92

Previously, our laboratory showed that human cytomegalovirus (HCMV) activates human immunodeficiency virus type 1 (HIV-1) in brain-derived cells with limited HIV-1 gene expression but inhibits HIV-1 in cells fully permissive for replication of both viruses (F. M. Jault, S. A. Spector, and D. H. Spector, J. Virol. 68:959-973, 1994). To investigate these effects further, we developed a model system that uncouples HIV-1 gene expression from long terminal repeat (LTR) activity. Two monoclonal U373-MG astrocytoma/glioblastoma cell lines (LTRIG and LIGHIVDC) were generated, each containing an integrated copy of an LTR-chloramphenicol acetyltransferase (CAT) construct and the Escherichia coli lacI gene. LIGHIVDC also has an inducible HIV-1 genome controlled by a Rous sarcoma virus promoter with lac operator sequences. Basal LTR-mediated CAT activity is 65-fold higher in LIGHIVDC than in LTRIG, and this activity is further increased (20-fold) following incubation of LIGHIVDC with isopropyl-beta-D-thiogalactopyranoside (IPTG). Tat protein can be detected by immunostaining in LIGHIVDC. However, Rev-mediated transport and subsequent translation of the singly spliced and unspliced HIV-1 mRNAs is inefficient. In the absence of Tat, HCMV stimulated CAT activity approximately 20-fold, and this activation required HCMV gene expression but not viral DNA replication. LTR-directed transcription was unaffected by HCMV infection in LIGHIVDC but was inhibited in these cells when they contained increased Tat levels following IPTG induction. These results support the hypothesis that HCMV can induce the HIV-1 LTR when HIV-1 gene expression is minimal and that a threshold level of HIV-1 gene products is necessary for HCMV to inhibit this promoter.
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PMID:A model system for human cytomegalovirus-mediated modulation of human immunodeficiency virus type 1 long terminal repeat activity in brain cells. 909 43