TBlack tea consumption and cancer risk: A prospective study
L. K. Heilbrun, A. Nomura & G. N. Stemmermann, Japan-Hawaii Cancer Study, Kuakini Medical Center, 347 N. Kuakini Street, Honolulu, H1 96817, USA.

In a prospective cohort study, men of Japanese ancestry were clinically examined from 1965 to 1968. For 7,833 of these men, data on black tea consumption habits were recorded. Since 1965, newly diagnosed cancer incidence cases have been identified: 152 colon 151 lung, 149 prostate, 136 stomach, 76 rectum, 57 bladder, 30 pancreas, 25 liver, 12 kidney and 163 at other (miscellaneous) sites. Compared to almost-never drinkers, men habitually drinking black tea more than once/say has an increased relative risk (RR) for rectal cancer (RR = 4.2). This positive association (P = 0.0007) could not be accounted for by age or alcohol intake. We also observed a weaker but significant negative association of black tea intake and prostate cancer incidence (P = 0.020). There were no significant associations between black tea consumption and cancer at any other site.

The Anti-Cancer Effects of Tea
Naasani-I, Seimiya-H, Tsuruo-T, Biochem-Biophys-Res-Commun 1998 Aug 19, Vol.: 249 (2), P: 391-6, ISSN: 0006-291X

Animal in vivo studies and human epidemiological observations indicated potent anticancer effects for tea. Here we demonstrate that epigallocatechin gallate (EGCG), a major tea catechin, strongly and directly inhibits telomerase, an enzyme essential for unlocking the proliferative capacity of cancer cells by maintaining the tips of their chromosomes. Telomerase inhibition was elaborated in a cell-free system (cell extract) as well as in living cells. In addition, the continued growth of two representative human cancer cell lines, U937 monoblastoid leukaemia cells and H29 colon adenocarcinoma cells, in the presence of non-toxic concentrations of EGCG showed life span limitations accompanied with telomere shortening, chromosomal abnormalities, and expression of the senescence-associated beta-galactosidase. It is suggested that telomerase inhibition could be one the major mechanisms underlying the anticancer effects of tea. Copywright 1998 Academic Press. Author

Polyphenols as cancer chemopreventive agents - a review.
Stoner, G.D., Mukhtar H., Journal of Cellular Biochemistry Supplement 22 169-180 1995

This article summarises available data on the chemopreventive efficacies of tea polyphenols, curcumin and ellagic acid in various model systems. Emphasis is placed upon the anticarcinogenic activity of these polyphenols and their proposed mechanism(s) of action. Tea is grown in about 30 countries and, next to water, is the most widely consumed beverage in the world. Tea is manufactured as either green, black, or oolong; black tea represents approximately 80% of tea products. Epidemiological studies, though inconclusive, suggest a protective effect of tea consumption on human cancer. Experimental studies of the antimutagenic and anticarcinogenic effects of tea have been conducted principally with green tea polyphenols (GTPs). GTPs exhibit antimutagenic activity in vitro, and they inhibit carcinogen-induced skin, lung, forestomach, oesophagus, duodenum and colon tumours in rodents. In addition, GTPs inhibit TPA-induced skin tumour promotion in mice. Although several GTPs possess anticarcinogenic activity, the most active is (-)-epigallocatechin-3-gallate (EGCG), the major constituent in the GTP fraction. Several mechanisms appear to be responsible for the tumour-inhibitory properties of GTPs, including enhancement of antioxidant (glutathione peroxidase, catalase and quinone reductase) and phase II (glutathion-S-transferase) enzyme activities; inhibition of chemically induced lipid peroxidation; inhibition of irradiation- and TPA-induced epidermal ornithine decarboxylase (ODC) and cyclooxygenase activities; inhibition of protein kinase C and cellular proliferation; anti-inflammatory activity; and enhancement of gap junction intercellular communication.

Curcumin is the yellow colouring agent in the spice turmeric. It exhibits antimutagenic activity in the Ames Salmonella test and has anticarcinogenic activity, inhibiting chemically induced preneoplastic lesions in the breast and colon and neoplastic lesions in the skin, forestomach, duodenum and colon of rodents. In addition, curcumin inhibits TPA-induced skin tumor promotion in mice. The mechanisms for the anticarcinogenic effects of curcumin are similar to those of the GTPs. Curcumin enhances glutathione content and glutathion-S-transferase activity in liver; and it inhibits lipid peroxidation and arachidonic acid metabolism in mouse skin, protein kinase C activity in TPA-treated NIH 3T3 cells, chemically induced ODC and tyrosine protein kinase activities in rat colon, and 8-hydroxyguanosine formation in mouse fibroblasts.

Ellagic acid is a polyphenol found abundantly in various fruits, nuts and vegetables. Ellagic acid is active in antimutagenesis assays, and has been shown to inhibit chemically induced cancer in the lung, liver, skin and oesophagus of rodents, and TPA-induced tumor promotion in mouse skin. Ellagic acid functions, through a variety of mechanisms, including inhibition of microsmal P-450 enzymes, stimulation of glutathione-S-transferase, scavenging the reactive metabolites of carcinogens, and direct binding to DNA, thus potentially masking sites that would normally interact with ultimate carcinogens.

GTP, curcumin and ellagic acid exhibit potent antioxidant effects. This property, coupled with their other effects, make them effective chemopreventives against both the initiation and promotion/progression stages of carcinogenesis.

Polyphenols may decrease diverse types of carcinogens
Weisburger-J-H, Hara-Y, Dolan-L, Luo-F-Q, Pittman-B, Zang-E, Mutat-Res 1996 Nov 4, VOL: 371 (1-2), P: 57-63, ISSN: 0027-5107

Previous research suggested that the mutagenicity of some genotoxic carcinogens, mainly heterocyclic amines, was decreased by green or black tea extracts, or tea polyphenol fractions. Thus, it seemed important to test a variety of genotoxic carcinogens with distinct chemical structures and means of biochemical activation as regards modification of mutagenicity in appropriate strains of Salmonella typhimurium by 3 concentrations of polyphenols 60, 100, or B, standard commercial polyphenol preparations from green or black tea. Polyphenols sharply decreased the mutagenicity of a number of aryl- and heterocyclic amines, of aflatoxin B1, benzo (a) pyrene, 1,2- dibromoethane, and more selectively, of 2-nitropropane, all involving an induced rat liver S9 fraction. Good inhibition was found with 2 nitrosamines that required a hamster S9 fraction for biochemical activation. No effect was found with 1-nitropyrene, and with the direct acting (no S9) 2-chloro-4-methyl-thiobutanoic acid. Thus, with some exceptions, polyphenols considerably decreased the mutagenicity of diverse types of carcinogens.