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Background   BRAF  and  K-ras  proto-oncogenes encode components of the ERK signalling pathway and are frequently mutated in colorectal cancer. This study investigates the associations between  BRAF  and  K-ras  mutations and clinicopathological, lifestyle and dietary factors in colorectal cancers.    Methods  186 adenocarcinomas and 16 adenomas from the EPIC Norfolk study were tested for  BRAF  and  K-ras  mutations. Diet and lifestyle data were collected prospectively using seven day food diaries.    Results   BRAF  V600E mutation was found in 15.6% of colorectal cancers but at higher frequencies in cancers with proximal location, poor differentiation and microsatellite instability (MSI) (all p < 0.001).  K-ras  mutation (mostly in codons 12 and 13) was found in 22.0% of colorectal cancers but at higher frequencies in cancers of more advanced Dukes' stage (p = 0.001), microsatellite stable (MSS) status (p = 0.002) and in individuals with lower blood high-density lipoprotein concentrations (p = 0.04). Analysis of dietary factors demonstrated no link between  BRAF  mutation and any specific dietary constituent, however,  K-ras  mutation was found at higher frequencies in individuals with higher white meat consumption (p < 0.001). Further analysis of specific mutation type demonstrated that G to A transitions in  K-ras  were observed at higher frequencies in individuals consuming lower amounts of fruit (p = 0.02).    Conclusion  These data support the model of  BRAF  and  K-ras  mutations arising in distinct colorectal cancer subsets associated with different clinicopathological and dietary factors, acting as mutually exclusive mechanisms of activation of the same signalling pathway.

bmc cancer

Dietary, lifestyle and clinicopathological factors associated with BRAF and K-ras mutations arising in distinct subsets of colorectal cancers in the EPIC Norfolk study