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Growth-stimulating Activity of Interleukin 6 on Human Mammary Epithelial Cells Transfected with the int-2 Gene¹

Institute of Pathological Anatomy, University of Pisa Medical School, 56100 Pisa [F. B., S. C., L. F.], and Institute of Medicine and Public Health, University of Pavia Medical School, 57, Viale Borri, 21100 Varese [P. G. C., V. F., A. T.], Italy

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.

¹ Supported by grants from the Italian Association for Cancer Research (Milan) and from the Istituto Superiore di Sanità (ISS-AIDS, Rome).

² To whom requests for reprints should be addressed.

Received 4/23/93. Accepted 5/28/93.