Research Article Polymorphisms of Homologous Recombination RAD51, RAD51B, XRCC2, and XRCC3 Genes and the Risk of Prostate Cancer Maria Nowacka-Zawisza, 1 Ewelina WiVnik, 1,2 Andrzej Wasilewski, 1,3 Milena SkowroNska, 1 Ewa Forma, 1 Magdalena BryV, 1 Waldemar RóhaNski, 4 and Wanda M. Krajewska 1 1 Department of Cytobiochemistry, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Poland 2 Department of Biophysics of Environmental Pollution, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Poland 3 Department of Biochemistry, Faculty of Medicine, Medical University of Lodz, 92-215 Lodz, Poland 4 2nd Department of Urology, Faculty of Biomedical Sciences and Postgraduate Training, Medical University of Lodz, 93-513 Lodz, Poland Correspondence should be addressed to Maria Nowacka-Zawisza; mnz@biol.uni.lodz.pl Received 29 April 2015; Revised 10 July 2015; Accepted 15 July 2015 Academic Editor: Francesco A. Mauri Copyright © 2015 Maria Nowacka-Zawisza et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Genetic polymorphisms in DNA repair genes may induce individual variations in DNA repair capacity, which may in turn contribute to the risk of cancer developing. Homologous recombination repair (HRR) plays a critical role in maintaining chromosomal integrity and protecting against carcinogenic factors. Te aim of the present study was to evaluate the relationship between prostate cancer risk and the presence of single nucleotide polymorphisms (SNPs) in the genes involved in HRR, that is, RAD51 (rs1801320 and rs1801321), RAD51B (rs10483813 and rs3784099), XRCC2 (rs3218536), and XRCC3 (rs861539). Polymorphisms were analyzed by PCR-RFLP and Real-Time PCR in 101 patients with prostate adenocarcinoma and 216 age- and sex-matched controls. A signifcant relationship was detected between the RAD51 gene rs1801320 polymorphism and increased prostate cancer risk. Our results indicate that the RAD51 gene rs1801320 polymorphism may contribute to prostate cancer susceptibility in Poland. 1. Introduction Prostate cancer (PC) is the second most commonly diagnosed malignant disease in men and the sixth leading cause of cancer-related death among men worldwide, with an esti- mated 10948 (14.3%) registered new cases and 4199 (8%) deaths in 2012 in Poland [1]. Although prostate cancer is one of the most common cancers in men, the genetic defects underlying its pathogenesis remain poorly under- stood. While being over 65 years and the presence of a family history are the strongest risk factors for prostate cancer, ethnicity has also been shown to be a risk factor, with the lowest incidence rates of prostate cancer being observed in Asian men, particularly in India, China, and Japan. Higher incidence rates are seen in black men. Te risk of developing prostate cancer is thought to be 1.3–2.0 times higher in African-American than Caucasian men [2]. Genetic defects in DNA repair and DNA damage res- ponse genes ofen lead to an increase of cancer incidence. Te most deleterious form of DNA damage is the DNA double- strand break (DSB), which can be formed by free radicals derived from the metabolism, ionizing radiation, or DNA cross-linking agents or which can naturally occur during DNA replication. Unrepaired DSBs lead to mutations, rear- rangements, and/or loss of chromosomes, causing genome instability and the development of tumors or cell death. In order to maintain genetic stability, DNA double-strand breaks must be repaired by homologous recombination or nonhomologous end-joining. Te key protein in homologous recombination is RAD51, which displaces replication protein A (RPA) and forms a helical nucleoflament on the exposed single-stranded DNA fanking the DSB. Tis nucleoflament performs a homology search for repair template and then catalyses DNA strand invasion [3, 4]. Hindawi Publishing Corporation Analytical Cellular Pathology Volume 2015, Article ID 828646, 9 pages http://dx.doi.org/10.1155/2015/828646