ABSTRACT
Colorectal cancer (CRC) remains the second most common malignancy in developed countries, accounting for approximately 20–30 deaths per 100 000 standard population each year, despite extensive knowledge of its epidemiology and molecular basis. The epidemiology and molecular biology underlying CRC have been studied more thoroughly and are better understood than for most neoplasias. Irreversible gene mutations are known to occur in a cell of colorectal mucosa in the initiation phase of CRC, followed by continued mutations, uncontrolled cellular proliferation and clonal expansion in the promotion phase. Progression involves genotypically altered cells developing the histological changes associated with CRC. The base-base mismatch repair system functions to identify and repair specific classes of errors in the DNA double helix, and is remarkably conserved in function and in enzymatic components from bacteria to humans. The exact location of a mutation within the adenomatous polyposis coli gene seems to be significant for the disease phenotype.
