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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
    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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  • 4
    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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  • 5
    Electronic Resource
    Electronic Resource
    Autocrine/paracrine regulation of keratinocyte urokinase plasminogen activator through the TGF-α/EGF receptor (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 155 (1993), S. 333-339 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Transforming growth factor-α (TGF-α) appears to be an important autocrine/paracrine regulator of keratinocyte function. Not only does TGF-α induce keratinocyte proliferation and migration in vitro, but it also has been detected in normal human epidermis and at elevated levels in hyperproliferative epidermis. In the present study we report that exogenous TGF-α increases urokinase-type plasminogen activator (uPA) in cultured human keratinocytes. Furthermore, in the absence of exogenous growth factors, the “basal” levels of uPA are decreased by an antagonist monoclonal antibody to the receptor shared by TGF-α and epidermal growth factor (EGF). These results suggest that an endogenous factor serves as an autocrine/paracrine regulator of keratinocyte uPA. We hypothesize that activation of the TGF-α/EGF receptor may coordinately regulate the keratinocyte response to cutaneous wounding, which includes enhanced uPA expression, migration, and proliferation. © 1993 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041550214
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  • 6
    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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