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Effects of type beta transforming growth factor in combination with retinoic acid or tumor necrosis factor on proliferation of a human glioblastoma cell line and clonogenic cells from freshly resected human brain tumors



Effects of type beta transforming growth factor in combination with retinoic acid or tumor necrosis factor on proliferation of a human glioblastoma cell line and clonogenic cells from freshly resected human brain tumors



Cancer Immunology Immunotherapy 26(3): 273-279



Type beta transforming growth factor (.beta.-TGF) is a potent regulator of cell growth and differentiation. The human glioblastoma cell line, T-MGI, was growth inhibited by .beta.-TGF under anchorage independent conditions. The antiproliferative effect of .beta.-TGF was potentiated to nearly total arrest by low doses of retinoic acid (RA) or tumor necrosis factor (TNF), while epidermal growth factor, platelet-derived growth factor, interleukin-2, and gamma interferon did not have this potentiating factor. The potentiation of the .beta.-TGF effect by RA and TNF could not be explained by the modulation of the epidermal growth factor receptor, the .beta.-TGF receptor, or the TNF receptor. .beta.-TGF alone and in combination with RA or TNF were further tested on primary cultures from freshly resected human gliomas biopsies (n = 13). There was great individual variation in sensitivity to .beta.-TGF, RA, or TNF. The astrocytoma and oligodendroglioma cells were inhibited to various degrees by .beta.-TGF or TNF, while most of the glioblastomas were not sensitive to these agents. Most of the biopsies were stimulated by RA. RA or TNF did not potentiate the growth inhibitory effect of .beta.-TGF on biopsy cells. We therefore think it unlikely that .beta.-TGF in combination with RA or TNF will be effective agents in the treatment of gliomas.

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Accession: 005332125

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PMID: 3164258

DOI: 10.1007/bf00199941


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