In the early stages of MAP tumourigenesis, a dominance of the BER defect can be concluded from the high frequency of G>T tranversions in KRAS2 and APC. In the later stages such G>T transversions seem less prominent, as seen in SMAD4 and p53. Mitotic recombination might be a driving force in MAP carcinogenesis, based on our conclusion that the LOH in MAP carcinomas mainly comprise copy neutral LOH. This evidence concerns the gene APC and familial adenomatous polyposis 2.