Diet, lifestyle and risk of K-ras mutation-positive and -negative colorectal adenomas

K-ras mutation-positive (K-ras⁺) and -negative (K-ras ^-) colorectal adenomas may differ clinically and pathologically. As environmental compounds may cause mutations in the growth-related K-ras oncogene or affect clonal selection depending on mutational status, we evaluated whether the aetiology of K-ras⁺ and K-ras^- adenomas differs. K-ras mutations in codons 12 and 13 were assessed in colorectal adenoma tissue (K-ras⁺: n = 81, K-ras^-: n = 453). Dietary and lifestyle data were collected through questionnaires that were also administered to 709 polyp-free controls. Multiple logistic regression analyses showed that intake of vitamin B2 and monounsaturated fat were differently associated with risk of K-ras⁺ and K-ras^- adenomas; vitamin B2 was inversely associated with K-ras^- (highest vs. lowest tertile: odds ratio (OR) = 0.70, 95% confidence interval (CI) = 0.50-0.97, p trend = 0.020), but not with K-ras⁺ adenomas, and a positive association with monounsaturated fat was confined to K-ras^- adenomas (OR = 1.57, 95% CI = 1.06-2.34, p trend = 0.029). Besides, potential, not statistically significant, differences in risk arose because red meat was distinctly positively associated with K-ras⁺ adenomas (OR = 1.70, 95% CI = 0.94-3.09, p trend = 0.061); total dietary and polyunsaturated fat tended to be inversely associated with risk of K-ras⁺ but not of K-ras^- adenomas; inverse associations with dairy products, calcium, protein and tea were confined to K-ras^- adenomas, and smoking was more markedly positively associated with K-ras^- adenomas. No differences in risk of K-ras and K-ras ^- adenomas could be detected for other factors. In conclusion, dietary and lifestyle factors may influence risk of K-ras⁺ and K-ras^- adenomas differently. However, epidemiological literature on diet, lifestyle and colorectal K-ras mutations is inconsistent.