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Conversely, WT-Bcr-Abl cells after treatment with N-Acetyl-Cysteine (NAC), a GSH precursor that increased the cellular GSH level, exhibited not only increased lengths of replication tracks but also insensitive to JMF4073 (Fig

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130 Due to the absence of the uricase enzyme responsible for converting uric acid into allantoin and allantoic acid, UA remains the terminal metabolic product in humans

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