Tea, particularly green tea, contains polyphenols like (-)-epigallocatechin-3-gallate (EGCG), which have been shown to inhibit tumor formation and growth in various animal models. These polyphenols exert their effects by suppressing cell proliferation, enhancing apoptosis, and inhibiting angiogenesis and metastasis. They act as antioxidants and can also generate reactive oxygen species (ROS), which may contribute to cancer prevention by binding to receptors and inhibiting key enzymes and signaling pathways. However, epidemiological studies on human cancer prevention have yielded inconclusive results, possibly due to confounding factors and varying tea consumption levels. Tea polyphenols, especially EGCG, have low bioavailability, which may limit their effectiveness. Studies in animal models suggest that tea can inhibit lung, oral-digestive tract, and prostate tumorigenesis. For example, EGCG reduced lung adenoma progression and inhibited tumor development in mice. In intestinal models, EGCG inhibited tumor formation by modulating signaling pathways. In colon cancer models, tea polyphenols reduced adenoma incidence and multiplicity. Human intervention studies have shown promising results, such as reduced cancer risk in tea drinkers. However, more well-designed studies are needed to confirm these findings. The mechanisms of tea's cancer-preventive effects include antioxidant activity, inhibition of signaling pathways, and modulation of enzyme activities. Despite these findings, the effectiveness of tea in humans remains uncertain due to factors like low consumption levels and confounding variables. Tea polyphenols may also influence cancer prevention through interactions with genetic polymorphisms and metabolic pathways. While some studies suggest that tea can reduce cancer risk, the results are inconsistent, and further research is needed to clarify the role of tea in cancer prevention. Overall, tea and its polyphenols show potential as cancer preventive agents, but more studies are required to fully understand their mechanisms and efficacy in humans.Tea, particularly green tea, contains polyphenols like (-)-epigallocatechin-3-gallate (EGCG), which have been shown to inhibit tumor formation and growth in various animal models. These polyphenols exert their effects by suppressing cell proliferation, enhancing apoptosis, and inhibiting angiogenesis and metastasis. They act as antioxidants and can also generate reactive oxygen species (ROS), which may contribute to cancer prevention by binding to receptors and inhibiting key enzymes and signaling pathways. However, epidemiological studies on human cancer prevention have yielded inconclusive results, possibly due to confounding factors and varying tea consumption levels. Tea polyphenols, especially EGCG, have low bioavailability, which may limit their effectiveness. Studies in animal models suggest that tea can inhibit lung, oral-digestive tract, and prostate tumorigenesis. For example, EGCG reduced lung adenoma progression and inhibited tumor development in mice. In intestinal models, EGCG inhibited tumor formation by modulating signaling pathways. In colon cancer models, tea polyphenols reduced adenoma incidence and multiplicity. Human intervention studies have shown promising results, such as reduced cancer risk in tea drinkers. However, more well-designed studies are needed to confirm these findings. The mechanisms of tea's cancer-preventive effects include antioxidant activity, inhibition of signaling pathways, and modulation of enzyme activities. Despite these findings, the effectiveness of tea in humans remains uncertain due to factors like low consumption levels and confounding variables. Tea polyphenols may also influence cancer prevention through interactions with genetic polymorphisms and metabolic pathways. While some studies suggest that tea can reduce cancer risk, the results are inconsistent, and further research is needed to clarify the role of tea in cancer prevention. Overall, tea and its polyphenols show potential as cancer preventive agents, but more studies are required to fully understand their mechanisms and efficacy in humans.