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Ultimately, within the oncogenic context, the JAB1/CRL4B complex acts as a master regulator of this plastic, coupled metabolic state, establishing a high-flux, adaptable network that supports rapid tumor proliferation and survival

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The endocrine and metabolic adaptation observed in both models may be a strategy to increase life span through a slower cell growing/metabolism, a slower loss of physiologic reserve capacity, a shift of cellular metabolism from cell proliferation to repair activities and a decrease in accumulation of senescent cells