AbstractThe effects of tea drinking on the tobacco‐specific nitrosamine 4‐(methylnitrosamine)‐1‐(3‐pyridyl)‐1‐butanone (NNK)‐induced mouse lung oncogene expression and the effect of topical application of the tea polyphenol component (‐)‐epigallocatechin‐3‐gallate (EGCG) on 12‐O‐tedradecanoylphorbol‐13‐acetate (TPA)‐induced mouse skin oncogene expression were investigated In the first experiment, mice were treated with NNK (1.3 mg/kg body wt ip) once a day for three days and were given 2% tea in drinking water during the whole experimental period. After four or eight weeks, the lung tissue of the mice treated with NNK displayed a significantly high level of expression in c‐myc, c‐raf, and c‐H‐ras oncogenes, and they were all inhibited by tea drinking with inhibitory rates of 50%, 20%, and 50%, respectively. In the second experiment, a single application of 10 nmol of TPA to mouse skin led to a marked increase in the transcripts’level of ornithine decarboxylase (ODC) gene, protein kinase C (PKC) gene, and c‐myc oncogene at four hours after TPA administration. Topical application of EGCG (1 or 5μmol) one hour before the application of TPA inhibited all TPA‐induced gene expression in a dose‐dependent fashion. These results confirm the anticarcinogenic effects of tea and suggest that a possible mechanism is the effect of tea on carcinogen‐induced oncogene expression.