Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We previously demonstrated that macrophages isolated from human malignant effusions support colony formation of autologous tumor cells in soft agar. We now demonstrate that macrophages (derived from effusions of patients with ovarian, breast, colon, or lung adenocarcinomas) secrete a soluble factor(s) that enhances the ability of a human epithelial tumor cell line (SW-13) to clone in soft agar. Macrophages increased colony growth 5 to 10-fold in a concentration dependent manner, although inhibition of cell growth was observed in the presence of high concentrations of macrophages. We attempted to increase production of tumor colony stimulating factor by exposing macrophages to lipopolysaccharide, concanavalin A, or phytohemagglutinin. Exposure of macrophages to these agents failed to increase their ability to secrete stimulatory factors. Macrophages were cultured for 1 day to 6 weeks in the presence of GCT-CM, a source of granulocyte-macrophage colony stimulating factor and the ability of these cultured macrophages to support colony growth assessed. The ability of macrophages to support colony growth declined gradually with time in culture reaching 50% of control values at 14 days, but remained at this level until 5 weeks of culture. The results of this study indicate the SW-13 cells may provide a quantitative assay for studying monocyte-derived tumor colony stimulating factors.
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PMID:Growth factors for human tumor clonogenic cells elaborated by macrophages isolated from human malignant effusions. 348 26

Several laboratories have reported marked tumor inhibition when the cytokine interleukin-10 (IL-10) is overexpressed as a transgene in a variety of tumor cells. To identify critical effector molecules, we compared the expression of the chemokine crg-2, the murine homolog of human inducible protein 10 (human IP-10) in murine mammary tumors derived from the transplantation of six IL-10 expressing clones of tumor cell line 66.1, parental 66.1, or 66-neo-cells. We observed increased levels of IP-10 mRNA in all IL-10-expressing tumors examined in comparison to 66-neo. IP-10 mRNA was not detected in parental 66.1 tumors. The closely related chemokine Mig (monokine induced by interferon-gamma [IFN-gamma]) was also induced in all IL-10-expressing tumors. Studies of cultured tumor cells in vitro show that mammary epithelial tumor cells, in the absence of host elements, can express IP-10 and Mig in response to induction with either lipopolysaccharide (LPS) or IFN-gamma alone. The combination of LPS plus IFN-gamma resulted in even greater induction of IP-10 RNA. The kinetics of induction differ somewhat for the two chemokines, with IP-10 showing slower induction and less rapid decline. Because both Mig and IP-10 are chemotactic for tumor-infiltrating lymphocytes, we examined the presence of CD4+ and CD8+ lymphocytes in these tumors. Consistent with the upregulation of Mig and IP-10, we saw significantly increased numbers of CD8+ cells and a lesser increase in CD4+ cells in tumors with elevated levels of both chemokines.
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PMID:Expression of the chemokines IP-10 and Mig in IL-10 transduced tumors. 1126 71

SUMMARY: Several laboratories have reported marked tumor inhibition when the cytokine interleukin-10 (IL-10) is overexpressed as a transgene in a variety of tumor cells. To identify critical effector molecules, we compared the expression of the chemokine crg-2, the murine homolog of human inducible protein 10 (human IP-10) in murine mammary tumors derived from the transplantation of six IL-10 expressing clones of tumor cell line 66.1, parental 66.1, or 66-neo-cells. We observed increased levels of IP-10 mRNA in all IL-10-expressing tumors examined in comparison to 66-neo. IP-10 mRNA was not detected in parental 66.1 tumors. The closely related chemokine Mig (monokine induced by interferon-gamma [IFN-gamma]) was also induced in all IL-10-expressing tumors. Studies of cultured tumor cells in vitro show that mammary epithelial tumor cells, in the absence of host elements, can express IP-10 and Mig in response to induction with either lipopolysaccharide (LPS) or IFN-gamma alone. The combination of LPS plus IFN-gamma resulted in even greater induction of IP-10 RNA. The kinetics of induction differ somewhat for the two chemokines, with IP-10 showing slower induction and less rapid decline. Because both Mig and IP-10 are chemotactic for tumor-infiltrating lymphocytes, we examined the presence of CD4+ and CD8+ lymphocytes in these tumors. Consistent with the upregulation of Mig and IP-10, we saw significantly increased numbers of CD8+ cells and a lesser increase in CD4+ cells in tumors with elevated levels of both chemokines.
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PMID:Expression of the Chemokines IP-10 and Mig in IL-10 Transduced Tumors. 1144 70