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Therefore, ferroptosis is better described as an accumulative process of lethal membrane-localized lipid peroxides instead of a type of oxidative stress
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Immune checkpoint molecules, tumor-associated macrophages, regulatory T cells, and myeloid-derived suppressor cells can attenuate the efficacy of ferroptosis and cuproptosis inducers, thereby forming a drug-tolerant microenvironment that promotes therapeutic resistance and early recurrence