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We propose that the dosage and duration of GSH administration in clinical treatment be carefully evaluated and standardized to prevent overuse and mitigate the risk of chemotherapy resistance

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BACH1 itself is a direct transcriptional target of HIF1A, which binds its promoter under hypoxic conditions to induce expression 174 , highlighting a multilayered transcriptional network linking hypoxia, GSH metabolism, and cuproptotic vulnerability

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