Abstract
Lung tumors are characterised has having high glucose and lactate use, and high heterogeneity in their metabolic pathways. Decades of research provides comprehensive knowledge of the rewired metabolic programs driven by oncogenic KRAS, including glucose metabolism, fatty acid synthesis, glutamine metabolism, autophagy signaling and redox homeostasis. KRAS mutations in non- small cell lung cancer (NSCLC) often occur with co-mutations in other genes such as TP53 and LKB1, and these co-existing genetic mutations can determine clinical response.
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