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A key mechanism underlying their therapeutic potential is the modulation of DNA topoisomerases, enzymes essential for DNA replication, transcription, and recombination. Inhibition of topoisomerase I and II induces DNA damage, replication stress, and apoptosis in rapidly proliferating cancer cells. Flavonoids such as quercetin, kaempferol, myricetin, and epigallocatechin\u20103\u2010gallate (EGCG) act as topoisomerase poisons or catalytic inhibitors by stabilizing the enzyme\u2010DNA cleavage complex, leading to DNA strand breaks. Additionally, their pro\u2010oxidant properties can enhance reactive oxygen species (ROS) generation, further amplifying DNA damage in tumor cells. Structural modifications of flavonoid scaffolds have improved enzyme selectivity, cellular uptake, and anticancer efficacy across various cancers, including leukemia, breast, colon, and lung cancer. 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