DNA damage and efficacy of DNA repair in patients with type 2 diabetes and coexisting colorectal cancer

INTRODUCTION Numerous epidemiological studies have indicated that the frequency of developing certain types of cancer, including colorectal cancer (CRC), is higher in patients with type 2 diabetes. The possible causes of this association have not been fully clarified. It has been suggested that chronic hyperglycemia‑related oxidative stress leading to oxidative DNA damage and impaired DNA repair may contribute to increased risk of cancer in type 2 diabetes.
OBJECTIVES The aim of the study was to evaluate the level of DNA damage and efficacy of DNA repair in patients with CRC with and without type 2 diabetes in comparison with healthy controls.

PATIENTS AND METHODS The alkaline comet assay was used to assess the level of endogenous oxidative and H2O2‑induced DNA damage and the efficacy of DNA repair in the lymphocytes of patients with type 2 diabetes, with CRC, with type 2 diabetes and CRC, and of healthy people (a total of 32 patients).

RESULTS The highest levels of endogenous oxidative and H2O2‑induced DNA damage were found in the lymphocytes of patients with type 2 diabetes and CRC. Additionally, the capacity of DNA repair was significantly decreased in patients with CRC with and without type 2 diabetes.
CONCLUSIONS Our findings support the hypothesis that an increased risk of cancer in type 2 diabetes may be associated with oxidative DNA damage; however, impaired DNA repair seems to play a major role in carcinogenesis in people with and without type 2 diabetes.