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By applying the quadratic multiomic metabolic transformation algorithm (qM 2 TA), we integrated metabolite and enzyme transcript levels to infer genome-scale metabolic rewiring upon treatment with Palbociclib, Telaglenastat, or their combination in vivo

Taken together, these elaborate mechanisms highlight the UPR not as a uniform survival pathway but as a dynamic, branch-specific signaling network whose outputs depend on tumor type, microenvironment, and stress duration