Nitric Oxide and Cancer: Pathogenesis and Therapy PDF download

Regulation of Cell Death Signaling by Nitric Oxide in Cancer Cells Jordi Muntané, Francisco Gallardo-Chamizo, Sheila Pereira, Ángela M. De los Santos, Ángeles Rodríguez-Hernández, Luís M. . · Yasuda, H. Solid tumor physiology and hypoxia-induced chemo/radio-resistance: novel strategy for cancer therapy: nitric oxide donor as a therapeutic enhancer. Nitric Oxide 19, Cited by: · There is growing evidence that patients with mitochondrial diseases have nitric oxide (NO) deficiency, and this can contribute to some of the complications observed in these patients. The best understood example is stroke-like episodes in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS.
Download full-text PDF. Read full-text ) References (71) Figures (2) Abstract and Figures. Nitric oxide (NO) is a pleiotropic regulator, critical to numerous biological processes, including. Nitric oxide can induce proliferation or apoptosis depending on the cellular context. Results suggest that the (CCTTT)n NOS2 microsatellite may influence bladder cancer risk and aggressiveness. This polymorphism may have an impact on disease pathogenesis, possibly by affecting intracellular nitric oxide levels. Abstract. Defining the specific role of nitric oxide (NO) in the regulation of the immune response against cancer is not a simple task. Despite of being extensively studied, NO, reactive nitrogen species (RNS) and reactive oxygen species (ROS) still maintain their reputation of "double-edge-swords".
Therapy of human ovarian cancer by transfection with the murine interferon beta gene: role of macrophage-inducible nitric oxide synthase. Hum Gene Ther ; – CAS Article Google Scholar. Gupta S, Ahmad N and Mukhtar H () Involvement of nitric oxide during phthalocyanine (Pc4) photodynamic therapy-mediated apoptosis. Cancer Res – CAS Google Scholar. Nitric oxide(NO) is a short-lived molecule required for many physiological functions, produced from Larginine by NO synthases (NOS). It is a free radical, producing many reactive intermediates that account for its bioactivity. Sustained induction of the inducible form of NOS (iNOS) in chronic inflammation may be mutagenic, through NO-mediated DNA damage or hindrance to DNA repair, and thus.
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