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Treatment with N-acetyl-L-cysteine, an antioxidant, or adenovirus-mediated overexpression of GPx1 attenuated the upregulation of adhesion molecules, confirming the role for GPx-1 suppression and hydrogen peroxide accumulation in these proinflammatory responses

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Given the need of tumor cells for glucose (for anaerobic glycolysis), GLN deficiency has been associated with cell death [12,13,14]