Alcoholic beverages and risk of renal cell cancer

Using a mailed questionnaire, we investigated the risk of renal cell cancer in relation to different types of alcoholic beverages, and to total ethanol in a large population-based case–control study among Swedish adults, including 855 cases and 1204 controls. Compared to non-drinkers, a total ethanol intake of >620 g month−1 was significantly related to a decreased risk of renal cell cancer (odds ratio (OR) 0.6, 95% confidence interval (CI) 0.4–0.9; P-value for trend=0.03). The risk decreased 30–40% with drinking more than two glasses per week of red wine (OR 0.6, 95% CI 0.4–0.9), white wine (OR 0.7, 95% CI 0.4–1.0), or strong beer (OR 0.6, 95% CI 0.4–1.0); there was a clear linear trend of decreasing risk with increasing consumption of these beverages (P-values for trends <0.05)

Functional and molecular effects of a green tea constituent on oral cancer cells

BACKGROUND: Green tea is heavily consumed on a global basis for its health benefits. The active ingredient, (-)-epigallocatechin gallate (EGCG), is a major polyphenol demonstrated to inhibit the growth of various non-oral cancer cell lines and interfere with the carcinogenic process, including downregulation of the epidermal growth factor receptor (EGFR). Our aim was to determine the phenotypic changes of oral cancer cells treated with EGCG and concurrently assess the effect on EGFR expression and activation. METHODS: Oral cancer cells (H400 and H357) were treated with 10 µg/mL and 20 µg/mL of EGCG for up to 72 hours. Phenotypic changes were assessed by performing cell proliferation analysis and cell migration (Transwell) assays. Expression of EGFR and its phosphorylated form (p-EGFR) was determined by Western blotting. RESULTS: Cell proliferation of both cell lines was significantly reduced at 48hrs when treated with 20 µg/mL EGCG. However, after 72 hours of treatment the effect of EGCG on cell proliferation ceased. Treatment of both cell lines with 10 µg/mL and 20 µg/mL of EGCG resulted in significant reduction in cell migration. Mechanistically, EGFR expression did not change significantly after treatment with EGCG; however, there was a reduction in its phosphorylated form. CONCLUSION: EGCG transiently inhibits both cell proliferation and migration of oral cavity cancer cells. This effect is associated with a decrease in the expression of phosphorylated EGFR. It is possible that more frequent bursts of EGCG could result in a persistent and sustained cancer inhibition, but this requires further research for clarification