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  • 1
    Electronic Resource
    Electronic Resource
    Stable Transfection of Human Malignant Melanoma Cells with Basic Fibroblast Growth Factor Antisense cDNA (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 660 (1992), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1992.tb21090.x
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  • 2
    Electronic Resource
    Electronic Resource
    Enhancement of epidermal growth factor receptor expression on glioma cells by recombinant tumor necrosis factor α (1992)
    Springer
    Cancer immunology immunotherapy 34 (1992), S. 370-376 
    Details
    ISSN: 1432-0851
    Keywords: Epidermal growth factor receptor ; Tumor necrosis factor ; Gliomas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recombinant tumor necrosis factor α (rTNFα; optimal dose 1000 U/ml) significantly increased the density of epidermal growth factor receptor (EGF-R) in three of four glioma cell lines in culture as determined by binding analysis of anti-EGF-R monoclonal antibody (mAb) 425. Since enhancement of EGF-R expression by rTNF-α was inhibited when cells were treated with the protein synthesis inhibitor cycloheximide, the effects of rTNFα may be protein-synthesis-dependent. The dose of rTNFα that was optimal for up-regulation of EGF-R on glioma cells did not inhibit the growth of these cells.125I-labeled mAb 425 lysed glioma cells in culture following its internalization into the cells. After glioma cells had been treated with rTNFα, the growth-inhibitory effects of the mAb were significantly enhanced, probably a reflection of the increase in EGF-R density on the tumor cell surfaces. The rTNFα effects were specific to the EGF-R and did not affect unrelated glioma-associated antigens. In our previous clinical trials,125I-labeled mAb 425 showed immunotherapeutic effects in glioma patients. The present study provides the basis for considerations of combined immunotherapy of glioma patients with125I-labeled mAb 425 and rTNFα.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01741746
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  • 3
    Electronic Resource
    Electronic Resource
    Melanoma-associated expression of vascular endothelial growth factor and its receptors FLT-1 and KDR (1999)
    Springer
    Journal of cancer research and clinical oncology 125 (1999), S. 621-629 
    Details
    ISSN: 1432-1335
    Keywords: Key words Melanoma ; Melanocytes ; VEGF ; flt-1 ; KDR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The expression patterns of vascular endothelial growth factor (VEGF) and its two receptors, flt-1 and KDR, were assessed in normal human melanocytes, transformed melanocytes expressing the simian virus 40 Tgene (SV40T), and melanoma cells derived from primary and metastatic lesions. Constitutive expression of VEGF, flt-1, and KDR mRNA and proteins was observed in the majority of primary and metastatic melanoma cell lines, and in SV40T-transformed melanocytes. VEGF expression in melanoma cell lines was further enhanced by exogenous growth factors including insulin and fetal calf serum. By contrast, neonatal melanocytes did not express VEGF or VEGF receptors and VEGF expression could not be induced by exogenous growth factors. Exogenous VEGF had no significant effects on melanoma cell proliferation or on production of a transcriptional target for VEGF, urokinase-type plasminogen activator. Down-regulation of VEGF expression in the metastatic melanoma cell line WM164 through transfection of a VEGF antisense construct similarly did not affect proliferation of the transfected cells in the presence or absence of exogenous VEGF. In summary, coexpression of VEGF and its receptors is a tumor-associated phenomenon in melanoma development. However VEGF production does not support autocrine proliferation of the melanoma cell lines tested.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004320050325
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  • 4
    Electronic Resource
    Electronic Resource
    Adenoviral transduction of melanoma cells with B7-1: antitumor immunity and immunosuppressive factors (1998)
    Springer
    Cancer immunology immunotherapy 46 (1998), S. 283-292 
    Details
    ISSN: 1432-0851
    Keywords: Key words B7-1 ; Adenovirus ; Melanoma ; T cell proliferation ; Immunosuppression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Previous studies in experimental models have demonstrated that the transduction of human or murine melanoma cells with the co-stimulatory B7-1 molecule induces effective antitumor immune responses. In order to develop B7-1 gene transfer as a therapeutic tool in the clinical management of melanoma, efficient means of in vivo gene transfer must be used. To this end we evaluated in vitro and in vivo immune responses associated with adenoviral transduction of murine and human melanoma cells with B7-1. Adenovirus-mediated transduction of human and murine melanoma cells with B7-1 leads to high-level transgene expression in vitro and in vivo and does not affect MHC class I and II expression. Adenovirus-delivered B7-1 induced antitumor immune responses, on the basis of observations that human melanoma cells transduced to express human B7-1 were able to co-stimulate allogeneic and autologous T cells to proliferate and that murine melanoma K1735 cells transduced to express murine B7-1 were rejected by syngeneic, immunocompetent mice. By contrast, intratumoral injection of an adenovirus encoding murine B7-1 failed to eliminate established murine melanoma (K1735) despite high-level transgene expression in tumor cells. Potent T cell inhibitory factor(s) secreted by both K1735 cells and select human melanoma cells may contribute to the failure to achieve protection in this setting. Thus, immune inhibitory melanoma-derived factors need to be taken into account when considering the clinical use of B7-1 immunotherapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002620050489
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  • 5
    Electronic Resource
    Electronic Resource
    T lymphocyte populations in multiple sclerosis (1985)
    Springer
    European archives of psychiatry and clinical neuroscience 235 (1985), S. 119 
    Details
    ISSN: 1433-8491
    Keywords: Multiple sclerosis ; Lymphocyte populations ; T4/T8 ratio and therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In 36 patients representing different clinical stages of multiple sclerosis (MS) (9 patients with acute exacerbations; 21 patients in remission; 5 patients with chronic progressive MS) determinations of T lymphocyte populations using monoclonal antibodies against surface antigens (OKT3 (pan T cells), OKT4 (helper T cells), OKT8 (cytotoxic/suppressor T cells)) were performed. Compared to the control group (40 healthy individuals) a clear elevation of the T4/T8 ratio was found in acute exacerbations and to a lesser degree in patients with inactive phases of MS. Patients with chronic progressive disease did not show increased T4/T8 ratios. Serial determination of lymphocyte populations after corticosteroid therapy in 10 selected patients revealed no significant changes which could be attribted to this therapeutic modality. Pathogenetic and clinical implications of the shifts in surface antigen expression of T lymphocyte populations mirroring the clinical course of MS are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00633483
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  • 6
    Electronic Resource
    Electronic Resource
    Growth factors in melanoma (1991)
    Springer
    Cancer and metastasis reviews 10 (1991), S. 89-101 
    Details
    ISSN: 1573-7233
    Keywords: melanoma ; growth factors ; autocrine ; paracrine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Human melanoma cells in culture are the source of a wide variety of polypeptide growth factors. Melanoma-derived basic fibroblast growth factor (bFGF), platelet-derived growth factor (PDGF)-A and PDGF-B chains, transforming growth factor (TGF)-α and TGF-β, interleukin (IL)-1α and IL-1β, and melanoma growth stimulatory activity (MGSA) have similar biochemical and functional properties when compared to their counterparts produced by untransformed cells. In contrast to melanoma cells, normal melanocytes, even under optimal growth conditions, express only TGF-β1 and MGSA at detectable levels suggesting that production of the other growth factors is a tumor-associated phenomenon. Recent evidence suggests that at least two of the growth factors, bFGF and MGSA, contribute to autocrine growth stimulation of melanoma cells. Whether PDGF, TGF-α, IL-1, and TGF-β act in an autocrine mode is unclear at present. However, these four growth factors are among those secreted by melanoma cells and, therefore, can be expected to interact with normal cells of the tumor stroma in vivo. Such paracrine effects include not only growth modulation in the context of angiogenesis and stroma formation, but also tissue degradation by proteolytic enzymes, the modification of extracellular matrix composition, and expression of adhesion receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00049407
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  • 7
    Electronic Resource
    Electronic Resource
    Growth factor independence and growth regulatory pathways in human melanoma development (1993)
    Springer
    Cancer and metastasis reviews 12 (1993), S. 219-226 
    Details
    ISSN: 1573-7233
    Keywords: melanoma ; cell lines ; tumor progression ; growth factors ; autocrine ; paracrine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This review concentrates on growth autonomy of tumor cells in relation to tumor progression. Human malignant melanoma serves as an example for progressive growth factor independence at subsequent stages of tumor progression. Mechanisms by which malignant cells acquire growth factor independence are discussed. In melanoma, deregulation of growth regulatory pathways has been described on four levels: 1) aberrant production of autocrine growth factors that substitute for exogenous growth factors (basic fibroblast growth factor [bFGF]); 2) alterations in the response to negative autocrine growth factors (interleukin [IL]-6 and transforming growth factor [TGF]-β); 3) overexpression of epidermal growth factor receptors (EGF-R); and 4) alterations of cellular protooncogenes involved in signal transduction (RAS, MYB) and growth suppression (p53). In addition to bFGF and IL-6, multiple other growth factor genes are activated in malignant melanoma cells but not normal melanocytes. These include both chains of platelet-derived growth factor (PDGF), TGF-α, IL-1, IL-8, and tumor necrosis factor (TNF)-α. Of these, PDGF-B has been investigated in more detail. Melanoma-derived PDGF clearly does not act in a direct autocrine mode, but has important paracrine effects on normal tissue constituents, notably fibroblasts and endothelial cells, that are essential for tumor developmentin vivo. It is speculated that other melanoma-derived growth factors with as yet undefined functions similarly exert such paracrine or ‘indirect’ autocrine effects that cannot be sufficiently addressed in studies on cultured cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00665954
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  • 8
    Electronic Resource
    Electronic Resource
    Monoclonal antibody 425 inhibits growth stimulation of carcinoma cells by exogenous EGF and tumor-derived EGF/TGF-α (1990)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 44 (1990), S. 69-79 
    Details
    ISSN: 0730-2312
    Keywords: carcinoma ; autocrine stimulation ; EGF-receptor ; transforming growth factor ; autocrine function ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Carcinoma cells frequently coexpress transforming growth factor (TGF)-α and its receptor, the epidermal growth factor (EGF) receptor, implicating an autocrine function of carinoma-derived TGF-α. Using a monoclonal antibody (425) to the EGF-receptor, we investigated the role of exogenous and tumor cell-derived EGF/TGF-α mitogenic activities in proliferation of cell lines derived from solid tumors. Monoclonal antibody 425 was chosen for these studies because it inhibits binding of EGF/TGF-α to the EGF-receptor and effectively blocks activation of the EGF-receptor by EGF/TGF-α. Seven malignant cell lines originating from carcinomas of colon, pancreas, breast, squamous epithelia, and bladder expressed surface EGF-receptor and secreted EGF/TGF-α-like mitogenic activities into their tissue culture media. All cell lines were maintained in a defined medium free of exogenous EGF/TGF-α. EGF and TGF-α added to the culture medium stimulated proliferation of five cell lines to comparable levels. EGF/TGF-α-dependent proliferation was significantly reduced by addition of MAb 425 to culture media. In addition, monoclonal antibody 425 reduced proliferation of the five EGF/TGF-α responsive cell lines in the absence of exogenous EGF/TGF-α. Antiproliferative effects induced by monoclonal antibody 425 were reversible and could be overcome by addition of EGF to culture media. Our results indicate that tumor-derived EGF-receptor-reactive mitogens can promote proliferation of carcinoma cells in an autocrine fashion.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240440202
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  • 9
    Electronic Resource
    Electronic Resource
    Interactions between growth factor receptors and corresponding monoclonal antibodies in human tumors (1987)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 35 (1987), S. 315-320 
    Details
    ISSN: 0730-2312
    Keywords: cancer ; growth regulation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Monoclonal antibodies (MAbs) to the human epidermal growth factor (EOF) receptor, the type I insulin-like growth factor (IGF) receptor, and the nerve growth factor (NGF) receptor were used to study the growth regulation of malignant cells. Anti-EGF receptor MAb 425 inhibited the growth of A 431 squamous carcinoma cells which express high numbers of EGF receptors on their surfaces. Growth inhibition induced by MAb 425 was accompanied by alterations of the cell-cycle distribution of these cells, indicating the ability of a monoclonal antibody to act as a biologically active ligand. Growth stimulation of melanoma cells by EGF was unrelated to EGF receptor expression on the cell surface. Insulin-and IGF-I-induced growth stimulation of melanoma cells was inhibited by MAb α-3 which reacts with the type I IGF receptor. This result indicates that the type I IGF receptor mediated growth stimulation not only by IGF-I but also by insulin. Normal melanocytes and cells of all stages of tumor progression expressed in tissue culture the receptor for NGF, but no effect on the growth of these cells has been observed.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240350406
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  • 10
    Electronic Resource
    Electronic Resource
    Induction of autocrine epidermal growth factor receptor ligands in human keratinocytes by insulin/insulin-like growth factor-1 (1995)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 163 (1995), S. 257-265 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Autocrine activation of the epidermal growth factor (EGF) receptor on keratinocytes has been recognized as an important growth regulatory mechanism involved in epithelial homeostasis, and, possibly, hyperproliferative diseases. Insulin-like growth factor (IGF)-1 and insulin have been shown to be paracrine keratinocyte mitogens that bind to the type I IGF receptor which is expressed on actively proliferating keratinocytes in situ. In this report, we demonstrate that IGF-1/insulin induced production of keratinocyte-derived autocrine growth factors that bind to the EGF receptor. Increased steady-state mRNA levels for transforming growth factor alpha (TGF-α) and for amphiregulin (AR) were observed upon incubation of keratinocytes with mitogenic concentrations of IGF-1. IGF-1 also induced production and secretion of TGF-α and AR proteins as detected by immunoassays. An EGF receptor antagonistic monoclonal antibody abolished the mitogenic effect of IGF-1 on cultured keratinocytes. These results suggest that stimulation of keratinocyte growth by IGF-1 requires activation of an EGF receptor-mediated autocrine loop. © 1995 Wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041630206
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