Abstract
We have shown recently that normal human mammary epithelial cells do produce interleukin 6 (IL6), interleukin 8, and a nonsecreted form of tumor necrosis factor. Here we report that ductal infiltrating mammary carcinomas fail to express immunoreactive IL6. Since abnormalities of cytokine genes are a frequent event in cancer, we investigated the production of and the response to cytokines of mammary cells using a panel of oncogene-transformed cells derived from the spontaneously immortalized MCF-10A cell line. We found that only the parental line and the int-2-transformed cells responded to exogenous IL6 and/or were suppressed by IL6-neutralizing antibody. In contrast to highly transformed cells, these two lines, which were either nontransformed (MCF-10A) or weakly transformed (int-2), were found to express IL6 receptors. These data suggest that loss of IL6 pathways can be a marker of mammary cell transformation.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Breast / metabolism
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Breast Neoplasms / genetics*
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Breast Neoplasms / metabolism
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Breast Neoplasms / pathology*
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Carcinoma, Intraductal, Noninfiltrating / genetics*
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Carcinoma, Intraductal, Noninfiltrating / metabolism
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Carcinoma, Intraductal, Noninfiltrating / pathology*
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Cell Division / drug effects
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Cytokines / biosynthesis
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Epithelium / metabolism
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Fibroblast Growth Factor 3
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Fibroblast Growth Factors / genetics*
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Genes, ras / genetics
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Humans
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Immunohistochemistry
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Interleukin-6 / biosynthesis
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Interleukin-6 / pharmacology*
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Interleukin-8 / biosynthesis
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Mice
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Proto-Oncogene Proteins / genetics*
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Receptor, ErbB-2
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Stimulation, Chemical
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Transfection
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Tumor Cells, Cultured
Substances
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Cytokines
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FGF3 protein, human
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Fgf3 protein, mouse
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Fibroblast Growth Factor 3
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Interleukin-6
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Interleukin-8
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Proto-Oncogene Proteins
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Fibroblast Growth Factors
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Receptor, ErbB-2