calcimycin and Lymphoma--T-Cell

We have previously reported that the growth of lymphocytes and tumor cells with lymphocyte lineage was strongly inhibited by a part of cloned macrophage hybridomas. This growth inhibition was accomplished by cell-to-cell contact and found to be attributed to lipid-like molecule(s) in a macrophage hybridoma cell membrane fraction. Instead of macrophage hybridomas, in the present study we utilized splenic adherent cells (SACs) that had been stimulated with IFN-gamma to see whether they inhibited tumor cell growth or not. The results demonstrated that IFN-gamma-stimulated but not unstimulated SACs showed a significant growth inhibition of BW-5147 tumor cells. This growth inhibition was not mainly mediated by prostaglandin E2 secreted from macrophages, since the inhibition was not reduced in the presence of indomethacin. Furthermore, as was reported previously in the case of macrophage hybridomas, the inhibitory activity resides in a lipid fraction of IFN-gamma-stimulated SAC membrane.

Topics: Animals; Antineoplastic Agents; Calcimycin; Cell Division; Cell Survival; Female; Humans; Interferon-gamma; Lipopolysaccharides; Lymphoma, T-Cell; Macrophage Activation; Macrophages; Membrane Lipids; Mice; Mice, Inbred DBA; Spleen; Tetradecanoylphorbol Acetate; Tumor Cells, Cultured