The immune system can inhibit or stimulate tumor growth. Peritoneal cells (PEG) from MM3 mammary tumor-bearing mice (TBM) displayed enhanced capacity to produce nitric oxide (NO) upon stimulation with LPS plus IFN-gamma, as compared to normal mice. The addition of L-Arginine (L-Arg) increased NO release by TBM-PEC but not by normal PEG; this increase could be reversed with N-G-nitro-L-arginine methyl ester (L-NAME). This inhibitor, given systemically, decreased MM3 tumor growth but not lung metastasis. Tumor retardation was associated with inhibition of angiogenesis induced by spleen cells. Conversely, L-Arg potentiated vascular response but not tumor growth. In conclusion, NO synthesis is up regulated in PEC during MM3 tumor progression sustaining tumor growth by mediating the angiogenic cascade.

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