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Specifically, mutant KRAS elevates ROS levels derived from mitochondria, which in turn induces acinar cells to undergo metaplasia into ductal epithelium, ultimately leading to the development of pancreatic intraepithelial neoplasia (104)

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Lkb1 and keap1/nrf2 pathways cooperatively promote metabolic reprogramming with enhanced glutamine dependence in kras-mutant lung adenocarcinoma

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