Mutator genes and mosaicism in colorectal cancer.

Recent studies have shed light on the role of defective DNA mismatch repair in human cancer. An elevated mutation rate associated with mismatch repair deficiency has been demonstrated in the germline and normal tissue from patients with hereditary non-polyposis colorectal cancer and transgenic animals respectively. Thus mismatch repair deficiency may permit the accumulation of mutations in cancer genes that do not confer growth advantage. This represents one potential mechanism for the induction of mutational mosaicism in humans.