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Mechanistically, the toxin exerts its carcinogenic effect through the formation of reactive epoxides that bind to DNA, oxidative stress generation, and interference with DNA repair pathways [168,169]

The positive circuit of NF-B activation and ROS production can accumulate more ROS in irradiated OSCC cells and this positive feedback regulation overcomes the pro-survival effect of NF-B/IL-6 signaling (90)