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As the efficacy of single-agent metabolic inhibitors is often limited by metabolic plasticity, developing rational combination therapies based on the coordinated targeting of oncogenic signaling and its downstream metabolic dependencies holds promise for systematically overcoming resistance and achieving more durable therapeutic benefits in tumors with specific genetic backgrounds

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Pey et al., 2014) and consequently, may have less profound implications for phenotype than the NQO1 * 2 polymorphism

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