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Crucially, the ROS generated during GSH degradation by CHAC1 may also cause further TP53 mutations, creating a vicious self-reinforcing cycle: CHAC1 activity promotes the very TP53 mutations that allow the tumor to exploit CHAC1s harmful effect for growth

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Targeting of vulnerabilities of drug-tolerant persisters identified through functional genetics delays tumor relapse

It has gained popularity because of its relationship to collagen-related pathways and its potential role in supporting healthy tissue signaling

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