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This indicates that mechanisms governing alternative substrate use, such as acetate, could be therapeutically targeted to enhance T cell activity in cancer (168)

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CJC-1295 and the GHRH pathway GHRH binds a G s -coupled receptor on pituitary somatotrophs, raising intracellular cAMP to drive synthesis and pulsatile release of GH, a system held in check by somatostatin (Mayo 2000)