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Induction of Iron-Nitric Oxide EPR Signals in Murine Cancers: Effects of Thiols and Cytokine-Induced Oxidant Stress

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Nitric Oxide in Transplant Rejection and Anti-Tumor Defense

Abstract

Murine lymphocytes incubated for three to four days with Interleukin-2 (IL-2) have enhanced tumoricidal activity and are called lymphocyte activated killer (LAK) cells (Lotze et al., 1981; Rosenstein & Rosenberg, 1984). When IL-2 has been administered to tumor-bearing mice or humans, dramatic anticancer responses were occasionally observed. The exact mechanism by which IL-2 mediates these in vivo responses is not yet clear, since LAK cells are not observed within tumors following IL-2 therapy. IL-2 treatment is also known to increase serum levels of inflammatory cytokines such as interferon-g (IFN-g), interleukin-1 (IL-1), and tumor necrosis factor (TNF) (Boldt et al., 1988; Gemlo et al., 1988). We have demonstrated that IL-2 induces NO synthesis in both mice and humans (Hibbs et al., 1992). Since IFN-g, IL-1, and TNF regulate the expression of the inducible/inflammatory nitric oxide synthase (iNOS) (Bastian et al., 1994), we have hypothesized that induction of nitric oxide synthesis may represent a potential antitumor mechanism that is activated by IL-2 therapy.

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© 1998 Springer Science+Business Media New York

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Bastian, N.R., Yim, CY., Hibbs, J.B., Samlowski, W.E. (1998). Induction of Iron-Nitric Oxide EPR Signals in Murine Cancers: Effects of Thiols and Cytokine-Induced Oxidant Stress. In: Lukiewicz, S., Zweier, J.L. (eds) Nitric Oxide in Transplant Rejection and Anti-Tumor Defense. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5081-5_19

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  • DOI: https://doi.org/10.1007/978-1-4615-5081-5_19

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-7311-7

  • Online ISBN: 978-1-4615-5081-5

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