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The timepoint chosen (when drug-tolerant cells are emerging after treatment) probably contributes to this effect, and later timepoints (when cells perhaps enter senescence or other more terminally arrested states) are more likely to reflect the expected gene expression patterns

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Specially, in breast cancer, oxidative stress is linked to DNA damage and mutations in key oncogenes and tumor suppressor genes, such as BRCA1 and TP53

Zelic et al., 2025)

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