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Introduction The term oxidative stress (OS) applies when increased amounts of reactive oxygen species (ROS) surpass the antioxidant (AOX) capacity that naturally offers the protective balance (1)

Several studies have shown that DNA hypermethylation in cancer cells targets tumor suppressor genes explicitly, resulting in growth selection and uncontrolled cell proliferation [25,26,27,28]

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Importantly, the Fenton reaction based on the release of Mn ions and the inactivation of GPX4 accompanied by accumulation of lipid peroxidation and ROS that can further sensitize Cuproptosis [173,174,175]

Both tumor and stromal cells release exosomes that carry specific addresses and are selectively internalized by recipient cells to modulate the TME locally or travel through the circulation to other organs [138]

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