Abstract
DNA repair represents a complex biological process that ensures genomic stability and integrity, consisting of several distinct pathways, repairing various types of DNA damage. DNA damage response is a complex pathway in response to DNA damage (involving, for instance, cell-cycle arrest, apoptosis, direct activation of DNA repair).
Unrepaired DNA damage and subsequent DNA damage response disruption are observed in many cancer types and it underlies the genomic instability, one of the hallmarks of cancer that accompanies tumorigenesis and cancer progression. Functional impairment of DNA damage response pathway has been found in many solid cancers.
In colon cancer, which belongs to the most frequent malignancies worldwide, hereditary syndromes with deficiencies in DNA mismatch repair and DNA repair polymerases have been described. Sporadic colon cancer exhibits multifactorial etiology, in which DNA repair mechanisms are important players involved in both cancer initiation and progression.
Moreover, modulations in DNA repair processes contribute to genetic heterogeneity and cancer evolution (genomic/chromosomal instabilities). Chemotherapy, one mode of systemic treatments in colon cancer patients, often utilizes increased vulnerability of rapidly dividing cells, including cancer cells, to DNA-damaging agents, resulting in overcoming DNA damage response and inducing cell death.
In this review we addressed the role of DNA repair in the prognosis and treatment prediction among patients with sporadic colon cancer. Particular attention has been dedicated to the determination DNA repair capacity in colon cancer patients that emerges as one of the most complex biomarkers, since it integrates a plethora of factors such as gene variants, gene expressions, the stability of gene products, the effect of inhibitors/stimulators, lifestyle and environmental factors.