%0 Journal Article %T Detection of Polymorphisms of DNA Repair Genes (XRCC1 and XPC) in Prostate Cancer %A Amani Fouad Sorour %A Iman Mamdouh Talaat %A Tamer Mohammed Abou Youssif %A Mohamed Adel Atta %J Journal of Cancer Therapy %P 1499-1505 %@ 2151-1942 %D 2013 %I Scientific Research Publishing %R 10.4236/jct.2013.410181 %X

Prostate cancer is a common disease with a multifactorial and complex etiology. It is the most common male malignancy and the second leading cause of death in many countries. The widespread use of PSA testing has increased the detection of this cancer at earlier stages, although this diagnostic method has proved to be insufficient to identify the disease. DNA in most cells is regularly damaged by endogenous and exogenous mutagens. At least four main partially overlapping damage repair pathways operate in mammals. Common polymorphisms in DNA repair genes may alter protein function and an individual¡¯s capacity to repair damaged DNA; deficits in repair capacity may lead to genetic instability and carcinogenesis. In the present study, we investigated the genotypic distribution of XRCC1 and XPC polymorphisms and its association with prostate cancer risk, pathological staging and Gleason¡¯s scoring. The present study was conducted in the departments of Clinical Pathology, Pathology, and Urology Faculty of Medicine, Alexandria University-Egypt. A total number of 50 patients with pathologically confirmed prostate cancer and 50 age-matched control subjects were enrolled in this study. The diagnosis was made on the basis of histopathological findings, following radical prostatectomy or transurethral resection of the prostate (TURP). Genomic DNA was extracted from peripheral blood using QIAamp blood DNA isolation kits. PCR followed by enzymatic digestion of the PCR products for (XRCC1, XPC) was used for the genotyping of these polymorphisms. Statistical analyses were performed using SPSS statistics version 20. The genotype frequencies of the studied polymorphisms in all the samples (n = 100), PC patients (n = 50) and healthy controls (n = 50) were consistent with %K Prostate Cancer %K Polymorphisms %K PCR %K XRCC1 %K XPC %U http://www.scirp.org/journal/PaperInformation.aspx?PaperID=41199