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Overall, these results indicated that the mitochondrial milieu constitutes a critical cellular target of aspirin

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doi: 10.1016/j.jfda.2016.10.016 430 KristoASKlimis-ZacasDSikalidisAK

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VKORC1L1 overexpression significantly attenuated tumor growth suppression in p53 wild-type tumors but not in p53-null tumors, suggesting a new pathway for p53-controlled ferroptosis and tumor growth inhibition mediated by vitamin K metabolism modulation

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