Approximately 90% of clear cell renal cell carcinomas (ccRCC) have biallelic inactivation of VHL, stabilizing HIFα and activating glycolytic genes, compromising mitochondrial metabolism.
In chromophobe RCCs, mutations in complex I of the electron transport chain contribute to mitochondrial dysfunction, while oncocytomas accumulate defective mitochondria from similar mutations.
Our findings emphasize that despite mitochondrial dysfunction in RCC, the actual impact on nutrient metabolism in vivo remains poorly understood, underscoring the need for further metabolic analysis.
The study found a consistent pattern of reduced glucose oxidation in ccRCCs, correlating with their progression and suggesting a metabolic adaptation during tumor growth.
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