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Taken together, these findings suggest that APR-246 could induce tumor cell death through both reactivation of mutant p53 and inhibition of cellular thiol-dependent redox system proteins (GPX4, TXNDR1, GRX1), providing novel combinatorial strategies for AML therapy

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[1] [2] These symptoms are related to the medication's effect on gastric motility rather than immune dysfunction

Collectively, ferroptosis might be a sensor in response to the pathophysiological alterations that disrupt the iron, ROS and inflammation homeostasis of our cardiovascular system