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Cancer cells’ plasticity provides the cell with the capability of switching between distinct stages of differentiation in order to survive in the tumor’s harsh microenvironment [9]

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AGEs following influx and accumulation in cells stimulate various signaling pathways, including TGF-β, c-Jun N-terminal kinase (JNK), MAPK/ERK, and NF-κB associated with inflammation, oxidative stress, and even different chronic metabolic diseases (90, 92)