Oxidative DNA damage and its repair are involved in pathogenesis of human cancers. The main pathway of oxidative DNA damage repair is base excision repair (BER). Functional studies performed on blood leukocytes have shown that some BER pathways may be decreased in cancer patients and this may be one of risk factors for the disease development. Decrease of 8-oxoG excision rate was observed in lung as well as head and neck cancer patients. Lung cancer patients revealed also lower rate of 1, N⁶-ethenoadenine (εA) excision rate, DNA damage induced by lipid peroxidation (LPO). Repair of another LPO-induced modification, 3,N⁴-ethenocytosine (εC) was decreased only in individuals developing lung adenocarcinoma, histological type of cancer, which ethiology is linked to inflammations. Activity of BER proteins is regulated by gene polymorphism, interaction of partner proteins and post-translational modifications. Polymorphism of DNA glycosylases may change their enzymatic activity. Some of these polymorphisms increase the risk of inflammation related cancers, e.g. colon, lung and other cancers. BER system efficiency may be also regulated by reactive oxygen species and diet, which stimulate transcription of some DNA glycosylases and the major human AP-endonuclease, APE1. The activity of repair enzymes may also be regulated by carcinogenic process. Stimulation of BER genes transcription or deregulation of repair proteins activity is frequently observed in cancer cells. Thus, modulation of BER proteins activity may be an important risk factor for cancer development, and may also contribute to cancer progression.

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1. Oxidative damage, DNA repair capacity and DNA repair gene polymorphisms and colon cancer.