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TNBC tumors exhibit marked metabolic plasticity, ranging from glycolytic phenotypes to OXPHOS-dependent states driven by peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α) signaling, mitochondrial biogenesis, and enhanced antioxidant buffering [49]

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Thiffault et al., 2000) and cells (Hartley et al., 1994