Inhibition of carcinogenesis by tea.
Tea has received a great deal of attention because tea polyphenols are strong antioxidants, and tea preparations have inhibitory activity against tumorigenesis. The bioavailability and biotransformation of tea polyphenols, however, are key factors limiting these activities in vivo. The inhibition of tumorigenesis by green or black tea preparations has been demonstrated in animal models on different organ sites such as skin, lung, oral cavity, esophagus, forestomach, stomach, small intestine, colon, pancreas, and mammary gland. Epidemiological studies, however, have not yielded clear conclusions concerning the protective effects of tea consumption against cancer formation in humans. The discrepancy between the results from humans and animal models could be due to 1) the much higher doses of tea used in animals in comparison to human consumption, 2) the differences in causative factors between the cancers in humans and animals, and 3) confounding factors limiting the power of epidemiological studies to detect an effect. It is possible that tea may be only effective against specific types of cancer caused by certain etiological factors. Many mechanisms have been proposed for the inhibition of carcinogenesis by tea, including the modulation of signal transduction pathways that leads to the inhibition of cell proliferation and transformation, induction of apoptosis of preneoplastic and neoplastic cells, as well as inhibition of tumor invasion and angiogenesis. These mechanisms need to be evaluated and verified in animal models or humans in order to gain more understanding on the effect of tea consumption on human cancer.
Yang
Chung S
CS
Laboratory for Cancer Research, Department of Chemical Biology, College of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey 08854-8020, USA. csyang@rci.rutgers.edu
Maliakal
Pius
P
Meng
Xiaofeng
X
D020533:Angiogenesis Inhibitors / Q000494:pharmacology; D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D002392:Catechin / Q000494:pharmacology; D002453:Cell Cycle / Q000187:drug effects; D005419:Flavonoids; D006801:Humans; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D009369:Neoplasms / Q000517:prevention & control*; D010636:Phenols / Q000493:pharmacokinetics / Q000494:pharmacology; D011108:Polymers / Q000493:pharmacokinetics / Q000494:pharmacology; D013662:Tea / Q000737:chemistry
D020533:Angiogenesis Inhibitors; D016588:Anticarcinogenic Agents; D000975:Antioxidants; D005419:Flavonoids; D016328:NF-kappa B; D010636:Phenols; D011108:Polymers; D013662:Tea; D002392:Catechin; D020928:Mitogen-Activated Protein Kinases