Abstract

Abstract Colon cancer is one of the important cancers in terms of morbidity and mortality. In U.S. alone, around 60,000 lives/year are lost to colon cancer. Diet and environment are implicated in the development of sporadic colon cancers. Our laboratory has already reported the development of colon tumors in ApcMin mice orally exposed to BaP. In this study we investigated the timing of RVT administration on BaP-induced colon carcinogenesis in ApcMin mice. The mice were grouped under 5 treatment categories. For Group I, only BaP was administered (in peanut oil) at a dose of 100 μg/kg via oral gavage over a 60 day period. For Group II, RVT (in 10% ethanol + 90% deionized water) was co-administered with BaP at a dose of 45 μg/kg. For Group III, RVT was administered for 1 week prior to BaP dosing. For Group IV, RVT was administered for 1 week post BaP dosing. The Vth group received RVT only. Jejunum, colon and liver samples were collected at the end of exposure; adenomas in the jejunum and colon were counted and subjected to histopathology. RVT significantly inhibited the development of adenomas in the jejunum and colon by 45 and 40 % (P < 0.001) respectively in Group II, compared to Group III (0 and 5%) and Group IV (0 and 2%). Though no significant difference was noted in the size of adenomas in jejunum of BaP + RVT-treated mice, compared to that of BaP-treated mice; the colon samples showed a different trend. RVT significantly reduced the size of colon adenomas in mice that received BaP & RVT simultaneously compared to mice that received BaP alone, RVT before BaP, and RVT post BaP. Though dysplasia of colon was observed in BaP-treated mice, it was of limited occurrence in RVT-treated mice. Our findings thus far reveal that the prevention colon tumorigenesis by RVT is effective only when given together with BaP, compared to prior and post BaP-exposure. Studies are in progress to see the underlying mechanisms for the differential preventive effects of RVT (funded by NIH grants 5T32 HL007735-14, RO3CA130112-01 and S11ES01415). Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2864.

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