Further evidence for the hypothesis was obtained by screening DNA from 124 individuals with multiple (from 3 to 100) colorectal adenomatous polyps for germline variants in a variety of genes involved in Wnt signaling (APC, AXIN1 and CTNNB1) and mismatch repair (MLH1 and MSH2)22. The overall frequency of variants in the individuals with adenoma was 24.9%, significantly higher than that of 11.5% in the controls. Each variant was also assessed for its possible functional effect, and essentially all satisfied the criteria one might expect22,23, as discussed later. Very similar overall results to those described above for colorectal adenomas have been found in a systematic study of the control of plasma levels of HDL cholesterol24.
