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Tumor cells expand mitochondrial adaptive reserve to resist stress and acquire therapeutic tolerance, whereas the common directionality of Sch B across multiple tumor models is compression of this mitochondrial adaptive reserve: by increasing oxidative burden to approach mitochondrial tolerance limits, disrupting ΔΨm and energy homeostasis to enhance the triggerability of death pathways, or weakening resistance-associated threshold-elevation mechanisms to potentiate therapeutic cytotoxicity
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This discrepancy limits the direct applicability of laboratory findings to real-world scenarios
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