The DNA repair system surveys the genome, which is always suffering from exposure to both exogenous as well as endogenous
mutagens, to maintain the genetic information. The fact that the basis of this DNA repair system is highly conserved, from prokaryote to mammalian cells, suggests the importance of precise genome maintenance mechanisms for organisms. In the past 15 years, considerable progress has been made in understanding how repair processes interact and how disruptions of these mechanisms lead to the accumulation of mutations and
carcinogenesis. In 1993, two groups reported that DNA mismatch repair could be associated with hereditary non-polyposis
colorectal cancer, indicating a connection between faulty DNA repair function and
cancer. More recently, an inherited disorder of
DNA glycosylase, which removes mutagenic oxidized base from
DNA, has been reported in individuals with a predisposition to multiple colorectal
adenomas and
carcinomas. This is the first report that directly indicates the role of the repair of oxidative
DNA in human inherited
cancer. Studies from gene knockout mice have elucidated the principal role of these repair systems in the process of
carcinogenesis. Moreover, clinical samples derived from
cancer patients have shown the direct involvement. This review focuses on the function of DNA mismatch repair and oxidative
DNA/
nucleotide repair among various DNA repair systems in cells, both of which are essentially involved in the
carcinogenesis of
gastrointestinal tract cancer.