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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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In GOLDEN 3 and 4, patients receiving either dose of GLY had lower incidences of AEs compared with placebo (Table 1)

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