Abstract
Abstract Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease with an extremely high lethality rate. Oncogenic KRAS activation has been proven to be a key driver of PDAC initiation and progression. There is increasing evidence that PDAC cells undergo extensive metabolic reprogramming to adapt to their extreme energy and biomass demands. Cell-intrinsic factors, such as KRAS mutations, are able to trigger metabolic rewriting. Here, we update recent advances in KRAS-driven metabolic reprogramming and the associated metabolic therapeutic potential in PDAC.
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