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Abstract Oncogenic MYC transcription factors profoundly rewire cellular programs, imposing therapeutically exploitable dependencies in MYC‑driven cancers such as high‑risk neuroblastoma. However, dissecting these synthetic lethal vulnerabilities using tunable gene expression remains challenging. Widely used tetracycline-regulated systems rely on inducers known to perturb mitochondrial function, introducing confounding off-target effects.
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