INHIBITORY EFFECT OF GREEN TEA EXTRACT ON THE PROCESS OF PANCREATIC CARCINOGENESIS INDUCED BY N-NITROSOBIS-(2-OXYPROPYL)AMINE (BOP) AND ON TUMOR PROMOTION AFTER TRANSPLANTATION OF N-NITROSOBIS-(2-HYDROXYPROPYL)AMINE (BHP)-INDUCED PANCREATIC-CANCER IN SYRIAN-HAMSTERS

Epidemiologic studies have shown a lower risk of gastrointestinal canc er in green tea drinkers. In the present study, the inhibitory effect of green tea extract (GTE) on the process of pancreatic carcinogenesis induced by N-nitrosobis-(2-oxypropyl)amine (BOP) and on tumor promoti on after transplantation of N-nitrosobis-(2-hydroxypropyl)amine (BHP)- induced pancreatic cancer were investigated in hamsters. In the first experiment, shortly after the initiation of pancreatic carcinogenesis by BOP, the animals in the GTE group were given GTE (0.5 mg/L) in thei r drinking water and the control group was given tap water. All animal s were sacrificed 24 weeks later. There were no significant difference s in body weight, water intake, or food consumption between the two gr oups during the experiments. GTE consumption was similar to 1.25 mg/da y/100 g body weight during this experiment. Seven of the 13 hamsters ( 54%) in the control group were found to have pancreatic tumors, versus six of the 18 hamsters (33%) in the GTE group. The average number of tumors in the control group was 1.0/hamster, compared with 0.5/hamster in the GTE group. The overall incidence of macroscopic pancreatic tum ors in the GTE group was about half that in the control group. The inc idence of pancreatic cancer was 54% (12/13) in the control group and 4 4% (8/18) in the GTE group. The number of pancreatic cancers, includin g invasive carcinoma and carcinoma in situ, in the GTE group was 0.88/ hamster, significantly lower than in the control group (1.68/hamster) (p < 0.05). The incidence of atypical ductal hyperplasia, which is tho ught to be an early pancreatic cancer, was also significantly lower in the GTE group than in the control group (1.50/hamster vs. 4.65/hamste r) (p < 0.05). In the second experiment, 1-mm(3) pieces of BHP-induced pancreatic cancer were transplanted into the back of hamsters. The co ntrol group (N = 16) was maintained on the basal diet and tap water th roughout the experiment, and the GTE group (N = 16) was also maintaine d on the basal diet and tap water for the first 3 weeks after transpla ntation, when successful transplantation was confirmed and, thereafter , given tap water containing GTE (0.5 mg/L) for an additional 12 weeks , Tumor growth was similar in both groups until 11 weeks after transpl antation, but inhibition of tumor growth became apparent after 11 week s in the GTE group. At 13 weeks, the average tumor volume in the GTE g roup was 1.01 +/- 0.11 x 104 mm(3), significantly smaller than that in the control group (1.98 +/- 0.37 x 104 mm(3)) (p < 0.05). The results demonstrated that GTE has an inhibitory effect on the process of panc reatic carcinogenesis and on tumor promotion of transplanted pancreati c cancer. These results suggest that GTE may come to serve as a chemop reventive and chemotherapeutic agent for pancreatic cancer.