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Mechanistically, macrophage-specific inhibition of GLUL leads to accumulation of succinate and HIF-1 via glutamine-dependent -aminobutyric acid (GABA) shunting (thereby inhibiting vessel sprouting and metastasis) and via stimulation of T effector cells

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Abstract Background Discrepancies in the utilization of reactive oxygen species (ROS) between cancer cells and their normal counterparts constitute a pivotal juncture for the precise treatment of cancer, delineating a noteworthy trajectory in the field of targeted therapies