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Role of immunoregulators as possibility of tumor hypoxia-induced apoptosis

R. Sharma, S. Kwon and C.J. Chen
Columbia University, US

tumor, hypoxia, cytokine, apoptosis, TNF-alpha

IL-1, TNF-α and INF-γ cytokines stimulate in nitric oxide production and result with inflammation manifested by apoptosis and hypoxia. We propose that extent of inflammation leading to hypoxia initially and programmed cell death later both can enhance the MRI visible edema fluid content in breast and lung tumors due to oxygen and energy insufficiency to surviving inflammatory tumor epithelial cells. The mechanism of A549 cell damage due to NO production included: Cytokines regulated NO synthase regulation through NF-kB cytosolic factor; Cofactor tetrahydrobiopterin-catalyzed synthesis of iNOS (inducible nitric oxide synthase. The NO production and increased NO synthase lead to Na+ ion transport and cell proliferation with differentiation or apoptosis. Our recent report on hypoxia-induced apoptosis and decreased cell proliferation with differentiation supported the possibility of MRI as potential technique in alveolar and tumor imaging of inflammation [1]. Hypoxic cells showed the possibility of NO production associated with their viability and rapid increase of apoptosis. High resolution MRI can track these high inflammation, tumor angiogenesis regions in tumors.
In conclusion, acute NO production can be a cause of hypoxia induced apoptosis and possibly MRI visible indicator of inflamed tumor viability.

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