Prostate cancer (PC) is one of the most common cancers and the second leading cause of mortality from cancer in Colombian men. Mitochondrial DNA (mtDNA) haplogroups have been associated with the risk of PC. Several studies have demonstrated dramatic differences regarding the risk of PC among men from different ethnic backgrounds. The present study was aimed at assessing the relationship between mtDNA haplogroups and PC. The mitochondrial DNA hypervariable segment I (HSV-1) was sequenced in a population-based study covering 168 cases (CA) and 140 unrelated healthy individuals as a control group (CG). A total of 92 different mtDNA sequences were found in CA and 59 were found in the CG. According to the geographical origin attributed to each mtDNA haplogroup, 82% of the mtDNA sequences found in both groups were Native Americans (A, B, C, and D). The most frequent was A (41.1%CA–42.1%CG), followed by B (22.0%CA–21.4%CG), C (12.0%CA–11.4%CG), and D (6%CA–10.0%CG). A lower percentage of European haplogroups (U, H, K, J, M, T, and HV) were also found (13.1%CA–12.9%CG), likewise African haplogroups (L0, L1, L2, and L3) (6.5%CA–2.1%CG). There were no statistically significant differences between the distribution of mtDNA haplogroups in CA and the CG in this study. 1. Introduction The precise molecular events leading to prostate carcinogenesis are currently not well known. The genetic characterization of this neoplasm has mainly been focused on the nuclear genome, showing complex chromosomal instability as one of the main changes; however, the cause of the diversity of chromosomal alterations detected in patients is still unclear. The presence of mutations in oncogenes and tumor suppressor genes has been associated with late events in the progression of prostate cancer (PC) [1]. Mitochondrial DNA (mtDNA) is the main target for cellular reactive oxygen species (ROS) and it has been observed that the level of oxidative damage is more extensive and persistent in this than in the nuclear genome, thereby leading to the accumulation of greater numbers of mutations [2]. Recent studies have shown that the presence of multiple homoplasmic point mutations in the mitochondrial genome is common in many human tumors, such as those found in colon and prostate cancers [3, 4]. These mutations could also lead to mitochondrial dysfunction due to alteration of the intermediary metabolism, which could be interpreted as a signal for inducing tumor pathogenesis [5]. The location of these mutations within the genome has been correlated with different types of cancer. The presence of
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