Extracts of tea, especially green tea, and tea polyphenols have been shown to inhibit the formation and development of tumours at different organ sites in animal models. There is considerable evidence that tea polyphenols, in particular (−)-epigallocatechin-3-gallate, inhibit enzyme activities and signal transduction pathways, resulting in the suppression of cell proliferation and enhancement of apoptosis, as well as the inhibition of cell invasion, angiogenesis and metastasis. Here, we review these biological activities and existing data relating tea consumption to human cancer risk in an attempt to understand the potential use of tea for cancer prevention.Dietary factors can substantially influence human cancer risk. Many food items, beverages and dietary constituents have reported cancer-preventive or anticancer activities. Tea, a commonly consumed beverage derived from the dried leaves of the Camellia sinensis plant, has been studied extensively for its health benefits, including cancer prevention. These studies are important because tea is consumed by a large proportion of the world's population and is the most popular beverage after water. Therefore, tea is the major source of dietary flavonoids (or polyphenols) in many populations. Tea is a unique food item in that the major constituents, especially those in green tea, are well characterized, allowing their biological activities to be thoroughly studied. The relationship between tea consumption and human cancer can be investigated using retrospective and prospective studies in which tea consumption is assessed by dietary recalls or by specific urinary markers.Although different aspects of tea and cancer prevention have been covered by previous reviews [1][2][3][4][5][6][7][8][9][10] , this Review critically assesses existing data and discusses our current understanding of how tea constituents might prevent cancer. We use selected recent findings to illustrate the types of laboratory results that are available. We also briefly review the results of human epidemiological and intervention studies, interpret these results on the basis of our understanding of the biochemical properties of tea constituents (BOX 1) and discuss possible mechanisms by which tea polyphenols prevent cancer development. Finally, we discuss the opportunities and challenges presented by the study of tea for cancer prevention. We hope that this Review will have wide-ranging implications, as many of the issues discussed here might also be applicable to studies of other dietary materials.Correspondence to: Chung S. Yang, csyang@rci.rutgers.edu. NIH Public Access Author ManuscriptNat Rev Cancer. Author manuscript; available in PMC 2010 March 1. Tea constituents and their biochemical propertiesThe major catechins (a group of polyphenols) in green tea are (−)-epigallocatechin-3-gallate (EGCG), (−)-epigallocatechin (EGC), (−)-epicatechin-3-gallate (ECG) and (−)-epicatechin (BOX 1). Tea catechins are characterized by the dihydroxyl or trihydroxyl substitutions on the B ring and the m-...

Tea made from the leaves of the plant Camellia sinensis is a popular beverage. The possible cancer preventive activity of tea and tea polyphenols has been studied extensively. This article briefly reviews studies in animal models, cell lines, and possible relevance of these studies to the prevention of human cancer. The cancer preventive activity of tea constituents have been demonstrated in many animal models including cancer of the skin, lung, oral cavity, esophagus, stomach, liver, pancreas, small intestine, colon, bladder, prostate, and mammary gland. The major active constituents are polyphenols, of which (-)-epigallocatechin-3-gallate (EGCG) is most abundant, most active, and most studied, and caffeine. The molecular mechanisms of the cancer preventive action, however, are just beginning to be understood. Studies in cell lines led to the proposal of many mechanisms on the action of EGCG. However, mechanisms based on studies with very high concentrations of EGCG may not be relevant to cancer prevention in vivo. The autooxidation of EGCG in cell culture may also produce activities that do not occur in many internal organs. In contrast to the cancer prevention activity demonstrated in different animal models, no such conclusion can be convincingly drawn from epidemiological studies on tea consumption and human cancers. Even though the human data are inconclusive, tea constituents may still be used for the prevention of cancer at selected organ sites if sufficient concentrations of the agent can be delivered to these organs. Some interesting examples in this area are discussed.

The present study investigated the inhibitory effects of Polyphenon E [a standardized green tea polyphenol preparation containing 65% (À)-epigallocatechin-3-gallate] and caffeine on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumor progression from adenoma to adenocarcinoma. Female A/J mice were treated with a single dose of NNK (103 mg/kg body weight, i.p.) and kept for 20 weeks for the mice to develop lung adenomas. The mice were then given a solution of 0.5% Polyphenon E or 0.044% caffeine as the sole source of drinking fluid until week 52. Both treatments significantly decreased the number of visible lung tumors. Histopathologic analysis indicated that Polyphenon E administration significantly reduced the incidence (by 52%) and multiplicity (by 63%) of lung adenocarcinoma. Caffeine also showed marginal inhibitory effects in incidence and multiplicity of adenocarcinoma (by 48% and 49%, respectively). Markers of cell proliferation, apoptosis, and related cell signaling were studied by immunohistochemistry, and the labeling index and staining intensity were quantified by the Image-Pro system. Polyphenon E and caffeine treatment inhibited cell proliferation (by 57% and 50%, respectively) in adenocarcinomas, enhanced apoptosis in adenocarcinomas (by 2.6-and 4-fold, respectively) and adenomas (both by 2.5-fold), and lowered levels of c-Jun and extracellular signal-regulated kinase (Erk) 1/2 phosphorylation. In the normal lung tissues, neither agent had a significant effect on cell proliferation or apoptosis. The results show that tea polyphenols (and perhaps caffeine) inhibit the progression of NNK-induced lung adenoma to adenocarcinoma. This effect is closely associated with decreased cell proliferation, enhanced apoptosis, and lowered levels of c-Jun and Erk1/2 phosphorylation. (Cancer Res 2006; 66(23): 11494-501)