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)

We have previously reported the tissue specific distribution of four different FGF-1 transcripts containing alternative 5' untranslated exons spliced to the first protein coding exon. The predominant transcript in brain is FGF-1.B and in kidney FGF-1.A. Others have shown, by in situ hybridization and immunohistochemical analysis, that expression of FGF-1 in the brain is exclusively in neural cells but not in glial cells. Here we have examined the distribution of FGF-1.B and FGF-1.A transcripts in glioblastoma and retinal tissues and in kidney carcinoma cell lines. Our results show that FGF-1.B is the predominant transcript in neural derived tissues including both the diabetic retina and normal retina tissues. Surprisingly, FGF-1.B transcript is highly expressed in glioblastoma tissues. In contrast, a normal brain glial cell line, CHII, expresses very low levels of FGF-1 mRNA. These results strongly implicate the role of FGF-1 in the etiology of glioblastoma. We also examined several kidney carcinoma derived cell lines for the expression of FGF-1 mRNA. Most of these kidney cell lines do not express any FGF-1 transcripts. An interpretation by deduction is that kidney adenocarcinomas are derived from cortex but medulla has been reported as the site of FGF-1 synthesis. Of the kidney derived cell lines which are positive for FGF-1 message, only one expressed FGF-1.A transcript. The data may suggest that the establishment of kidney cell lines results in a switch of promoter usage from the 1.A seen in kidney tissue. Similarly, culturing of glioma cell lines may result in a switch from FGF-1.B seen in glioma tissues to FGF-1.D seen in most glioma cell lines. Continued studies of the FGF-1 transcripts, their functional promoters and their tissues distribution will provide insight into the potential role of FGF-1 in cell growth, tissue differentiation and malignant transformation.
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PMID:Different fibroblast growth factor 1 (FGF-1) transcripts in neural tissues, glioblastomas and kidney carcinoma cell lines. 754 53

In the search for cytokines whose antiproliferative action could be enhanced by combination with dipyridamole, 2,6-bis(diethanolamino)-4,8-dipiperidinopyrimido[5,4-d]pyrim idine, the combination of tumor necrosis factor-alpha (TNF-alpha) with this agent was evaluated in various human tumor cell lines. Inhibition of the proliferation of human melanoma cell lines MM-1CB and HMV-1 by TNF-alpha (1-10(2) U/ml) was enhanced in culture dishes by combination treatment with dipyridamole (0.1-10 microM). The enhancement effect was also detected in other tumor cell lines: T98 (glioma), SCC-1CB (squamous cell carcinoma), HAC-2 (ovarian clear-cell carcinoma), HLE (hepatoma), HEC-1 (endometrial adenocarcinoma) and HOC-21 (ovarian serous cystadenocarcinoma). The incorporation of [14C]amino acids and [3H]uridine into acid-insoluble cell materials in the combination-treated cells was not significantly different from that in cells treated with TNF-alpha or dipyridamole. However, the incorporation of [3H]thymidine was specifically inhibited in all cell lines examined after more than 12 h of the TNF-alpha and dipyridamole combination treatment, although neither agent alone inhibited this incorporation. On the other hand, the growth of tumors induced by the injection of MM-1CB and HMV-1 cells into nude mice was more markedly inhibited by the subcutaneous administration of TNF-alpha in combination with orally administered dipyridamole than by either agent alone. The results presented suggested that dipyridamole is beneficial in assuring the effectiveness of anti-cancer cytokine therapy.
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PMID:Dipyridamole combined with tumor necrosis factor-alpha enhances inhibition of proliferation in human tumor cell lines. 755

Cluster of differentiation 15 (CD15) monoclonal antibodies recognise cell adhesion molecules on the surface of many cells including normal astrocytes and metastatic carcinoma cells. The CD15 epitope (fucosyl-N-acetyl-lactosamine), an adhesive oligosaccharide, functions as a ligand for the selectin family of membrane receptors. These include CD62, a cytokineinducible glycoprotein found in platelets and endothelial cells. CD15 is one of a series of putative adhesion molecules expressed in nervous tissue. Selectin-carbohydrate interactions have been implicated in the metastatic spread of cancer cells. We have immunostained a variety of cultured human brain tumours, three cell lines derived from experimental rat gliomas, two specimens of cultured human foetal astrocytes, two metastatic carcinoma cell lines and human umbilical vein endothelial cells (HUVEC) using two monoclonal antibodies which recognise CD15. While all of the animal glioma cells were positive for CD15, only two human glioma cell lines, derived from an anaplastic astrocytoma and a glioblastoma multiforme, respectively, displayed limited reactivity. Chromium radiolabel binding assays of CD15-positive and -negative cell lines including glioma and carcinoma-derived cells, using HUVEC as an attachment substrate, were carried out in the presence and absence of CD15 monoclonal antibody. The level of adhesion of neoplastic cells to HUVEC not only corresponded to CD 15 expression but application of anti-CD 15 monoclonal antibodies considerably reduced adhesion. We postulate that the absence of CD15 on human glioma cells may explain, to some extent, the general failure of intrinsic brain tumours to metastasis by precluding the adhesion of circulating neoplastic glia to 'target' organ endothelium.
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PMID:Nonexpression of CD15 by neoplastic glia: a barrier to metastasis? 765 94

Three different classes of Fc receptors for IgG (Fc gamma R) are currently distinguished in humans, of which polymorphonuclear phagocytes (PMN) normally express both low-affinity receptor classes--Fc gamma RII (CD32) and Fc gamma RIII (CD16). During therapy with granulocyte colony-stimulating factor (G-CSF), neutrophils from patients with various malignancies and different hematologic disorders were found to additionally express high levels of the receptor with high affinity for IgG (Fc gamma RI; CD64). For these patients, the relative fluorescence intensity (rFI) for Fc gamma RI was 5.3 (range, 1.7 to 10.3; n = 19), compared with 1.0 (range, 1.0 to 1.1; n = 8) for healthy donors. The expression of Fc gamma RI during G-CSF therapy could be confirmed by using a panel of six CD64-specific antibodies, and by showing mRNA for Fc gamma RI. So far, three genes for Fc gamma RI have been identified, encoding four distinct transcription products. By reverse transcriptase-polymerase chain reaction technology, transcripts for both membrane-associated isoforms (hFc gamma RIa and hFc gamma RIb2) could be detected. The functional activity of Fc gamma RI on PMN during G-CSF therapy was shown by measuring binding of monomeric human IgG and antibody-dependent cellular cytotoxicity (ADCC). Thus, Fc gamma RI-positive neutrophils displayed enhanced ADCC activity to glioma (A1207), squamous cell (A431), and ovarian (SK-ov3) carcinoma cell lines. The involvement of Fc gamma RI in this increased cytotoxic activity was shown by blocking Fc gamma receptors with monoclonal antibodies, and by using F(ab')2 x F(ab')2-bispecific antibodies with specificities against tumor-related antigens and Fc gamma RI, resulting in solely Fc gamma RI-mediated cytotoxicity. Therapeutically, this additional Fc receptor on PMN may increase the efficacy of experimental antibody therapy.
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PMID:Involvement of the high-affinity receptor for IgG (Fc gamma RI; CD64) in enhanced tumor cell cytotoxicity of neutrophils during granulocyte colony-stimulating factor therapy. 768 98

To identify potential cell surface receptors for chicken cytotactin (CT), we have characterized the ability of recombinant fusion proteins spanning the proximal fibronectin (FN) type III repeats of the molecule to support attachment of glioma and carcinoma cell lines. The third FN type III repeat, which contains the RGD tripeptide, supported cell attachment and cell spreading; however, mutation of RGD to RAD did not result in significant loss of either activity. In addition, the same repeat of mouse CT, which contains a natural mutant, RVD, also supported cell attachment and spreading, although at a lower level; both activities were increased by mutation of the RVD sequence to RGD. Studies utilizing RGD-containing peptides and well-characterized antibodies to integrins indicated that cell attachment to the third FN type III repeat was mediated by at least two different integrin receptors of the alpha v subtype. Additional cellular receptors may also be involved in cell attachment to CT. For example, an antibody to the beta 1 subfamily of integrins partially inhibited binding of cells to intact CT but did not inhibit cell binding to the third FN type III repeat. These findings suggest that the RGD site in CT is able to mediate cell attachment to integrins and thus is not a cryptic adhesion site. They also open the possibility that the functions of CT in processes such as counteradhesion, cell migration, cell proliferation, and cell differentiation may be mediated in part by interaction with multiple integrins.
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PMID:Multiple integrins mediate cell attachment to cytotactin/tenascin. 769 84

Removal of histones and other nuclear proteins greatly enhances the sensitivity of mammalian cells to DNA damage by ionizing radiation. We examined the possibility that the ease of dissociation of histones, or the association of other nuclear proteins with DNA, may differ between radioresistant and sensitive human tumor cells. Cells embedded in agarose were exposed to increasing salt concentrations prior to irradiation and examination using a microscopic gel electrophoresis method, the neutral comet assay. Induction of double-strand breaks increased by a factor of about 20 when cells of four human tumor cell lines, HT144 melanoma, HT29 adenocarcinoma, DU145 prostate carcinoma and U87 glioma, were exposed to 2 M NaCl prior to irradiation. Subtle differences in sensitivity to induction of double-strand breaks by radiation between cells of the four cell lines were also observed after extraction with 0.7-1.1 M NaCl; however, no correlation with radiosensitivity was apparent. While a significant number of histone and non-histone proteins are present after extraction with 1.2 M NaCl, these proteins apparently have only a minor influence on radiosensitivity. However, if they are allowed to remain with DNA during electrophoresis, about 15 times more strand breaks are required to produce a similar amount of DNA migration in both DU145 and HT144 cells. These results suggest that the association between proteins and DNA within the nucleus, as probed by extraction with sodium chloride, does not help to explain differences in intrinsic radiosensitivity among cells of these diverse tumor cell lines.
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PMID:Radiation-induced DNA double-strand breaks produced in histone-depleted tumor cell nuclei measured using the neutral comet assay. 772 28

The 1-acyl- and 1,2-diacyl-4,4-diethyl-3,5-pyrazolinediones proved to be cytotoxic against the growth of a number of cell lines, including murine and human leukemias. HeLa suspended carcinoma, colon adencarcinoma SW480, KB nasopharynx and glioma tumors. Selected compounds were also active in the human lung bronchogenic MB-9812, and osteosarcoma TE418 screens. These derivatives were active in vivo in the Ehrlich ascites carcinoma screen in CF-1 mice at 8 mg/kg/day I.P. The mode of action in Tmol3 leukemia cells showed that the compounds reduced de novo synthesis of purines and pyrimidines and inhibited dihydrofolate reductase and ribonucleoside reductase activities. The DNA molecule was not a target although limited DNA strand scission may be possible.
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PMID:The cytotoxic activity of 1-acyl- and 1,2-diacyl-4,4-diethyl-3,5-pyrazolidinediones. 773 34

The murine MAb 425 (IgG2a) directed against human epidermal growth factor receptor is considered to have therapeutic potential in glioma patients. In order to circumvent immune response in clinical use, the MAb 425 was humanized by CDR-grafting (IgG1). We have studied the distribution of reshaped MAb 425 (EMD 62,000) in Wistar rats and the specific localization in female nude mice bearing human mamma carcinoma xenografts. The 125I-labelled MAb 425 was administered intravenously in a single dose (1 mg/kg) using unspecific human IgG1 antibody as control. The biodistribution was investigated both quantitatively and by whole-body autoradiography. The autoradiographs showed a selective uptake of radioactivity by the tumour tissue. 15 days after administration, radioactivity was bound exclusively to the tumour. Similar results were obtained with the murine monoclonal antibody. Quantitative studies exhibited a tumour-blood ratio of about 5. The study demonstrates that the humanized MAb 425 is selectively localized in human mamma carcinoma xenografted to athymic mice.
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PMID:Distribution of humanized MAb 425 (EMD 62,000) in rats and specific localization in tumor-bearing nude mice. 777 32

We have identified and sequenced a new gene from human cells that is responsive to DNA damage and retinoic acid treatment, and it is highly expressed in brain and reproductive organs (BRE). This BRE gene encodes an mRNA of 1.7-1.9 kb, with an open reading frame of 1,149 bp, and gives rise to a deduced polypeptide of 383 amino acid residues. Treatment of fibroblast cell with UV and 4-nitroquinoline-1-oxide caused more than 90% and 50% decreases in BRE mRNA, respectively. Similar decreases in BRE expression were observed in RA-treatment of the brain glioma cell U-251 and the promyelocytic cell HL-60. Decrease in BRE mRNA was also observed in a squamous carcinoma cell, 1483, that showed X-ray resistance and has a more aggressive tumorigenic phenotype, but BRE expression was unchanged in cells after growth inhibition. These data indicate that BRE is a house-keeping gene and it may play a role in homeostatis or in certain pathways of differentiation in cells of neural, epithelial and germ line origins.
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PMID:Identification of a brain- and reproductive-organs-specific gene responsive to DNA damage and retinoic acid. 782 98

The proliferation of normal non-tumourigenic mouse fibroblasts is stringently controlled by regulatory mechanisms located in the postmitotic stage of G1 (which we have designated G1pm). Upon exposure to growth factor depletion or a lowered de novo protein synthesis, the normal cells leave the cell cycle from G1pm and enter G0. The G1 pm phase is characterized by a remarkably constant length (the duration of which is 3 h in Swiss 3T3 cells), whereas the intercellular variability of intermitotic time is mainly ascribable to late G1 or pre S phase (G1ps) (Zetterberg & Larsson (1985) Proc. Natl. Acad. Sci. USA 82, 5365). As shown in the present study two tumour-transformed derivatives of mouse fibroblasts, i.e. BPA31 and SVA31, did not respond at all, or only responded partially, respectively, to serum depletion and inhibition of protein synthesis. If the tumour cells instead were subjected to 25-hydroxycholesterol (an inhibitor of 3-hydroxy-3 methyglutaryl coenzyme A reductase activity), their growth was blocked as measured by growth curves and [3H]-thymidine uptake. Time-lapse analysis revealed that the cells were blocked specifically in early G1 (3-4 h after mitosis), and DNA cytometry confirmed that the arrested cells contained a G1 amount of DNA. Closer kinetic analysis revealed that the duration of the postmitotic phase containing cells responsive to 25-hydroxycholesterol was constant. These data suggest that transformed 3T3 cells also contain a 'G1pm program', which has to be completed before commitment to mitosis. By repeating the experiments on a large number of tumour-transformed cells, including human carcinoma cells and glioma cells, it was demonstrated that all of them possessed a G1pm-like stage. Our conclusion is that G1pm is a general phenomenon in mammalian cells, independent of whether the cells are normal or neoplastic.
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PMID:Existence of a commitment program for mitosis in early G1 in tumour cells. 783 84


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