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Although the incidence of gastric cancer (GC) has declined substantially in the past few decades, it remains the fifth most common cancer and the third most frequent cause of cancer deaths worldwide (1,2). GC is multifactorial, and it is very important to develop reliable biomarkers for predicting the risk of GC to maximize therapeutic effects and to minimize adverse effects of treatment. Many studies have evaluated the roles of nuclear DNA alterations in gastric tumorigenesis; however, relatively less attention has been paid to mitochondrial DNA (mtDNA) alterations (3). The proximity of the mitochondrial genome to reactive oxygen species production sites, limited repair mechanisms, and a lack of protective histone proteins all result in a higher mutation rate in the mitochondrial genome than in the nuclear genome (4). In the present study, we have identified associations between mutations in the D-Loop and a wide variety of cancers, including GC, colorectal cancer, nonHodgkin’s lymphoma, non-small cell lung cancer and breast cancer, etc., but associations involving polymorphisms in mtDNA coding regions remain largely unknown (5-9). Mitochondrial cytochrome c oxidase (MT-CO) genes (including MT-CO1, MT-CO2 and MT-CO3) encode three subunits of respiratory complex IV, a key enzyme in aerobic metabolism. Mutations in MT-CO genes may Original Article

Identification of polymorphisms in mitochondrial cytochrome c oxidase genes as risk factors for gastric cancer