Toward a Unifying Hypothesis for Redesigned Lipid Catabolism as a Clinical Target in Advanced, Treatment-Resistant Carcinomas

The document reviews the role of redesigned lipid metabolism in advanced, treatment-resistant carcinomas, proposing the "lipid metabolism resistance system" (LMRS) hypothesis. This hypothesis suggests that enhanced lipid catabolism in carcinoma cells provides increased energy and reduces potential, aiding in survival and treatment resistance. The review highlights the importance of peroxisomal beta-oxidation and the enzyme SCD1 in sustaining carcinoma cell behavior. Evidence from various studies shows that inhibiting these pathways with agents like thioridazine and crizotinib can sensitize resistant carcinoma cells to treatments. The findings suggest that targeting the LMRS pathway could improve clinical outcomes by overcoming treatment resistance in advanced carcinomas.