Bladder Cancer and Polymorphisms of DNA Repair Genes (XRCC1, XRCC3, XPD, XPG, APE1, hOGG1)

• Published in: Anticancer research 2009-04, Vol.29 (4), p.1389-1393
• Main Authors: NARTER, Kamil Fehmi, ERGEN, Arzu, AGACHAN, Bedia, GÖRMÖS, Uzay, TIMIRCI, Ozlem, ISBIR, Turgay
• Format: Article
• Language: English
• Subjects: Adenocarcinoma - genetics; Adenocarcinoma - secondary; Adult; Aged; Aged, 80 and over; Biological and medical sciences; Carcinoma, Transitional Cell - genetics; Carcinoma, Transitional Cell - secondary; Case-Control Studies; DNA Glycosylases - genetics; DNA Repair; DNA Repair Enzymes - genetics; DNA-(Apurinic or Apyrimidinic Site) Lyase - genetics; DNA-Binding Proteins - genetics; Endonucleases - genetics; Female; Humans; Male; Medical sciences; Middle Aged; Nephrology. Urinary tract diseases; Nuclear Proteins - genetics; Polymerase Chain Reaction; Polymorphism, Genetic - genetics; Polymorphism, Restriction Fragment Length; Transcription Factors - genetics; Tumors; Tumors of the urinary system; Urinary Bladder Neoplasms - genetics; Urinary Bladder Neoplasms - pathology; Urinary tract. Prostate gland; X-ray Repair Cross Complementing Protein 1; Xeroderma Pigmentosum Group D Protein - genetics
• ISSN: 0250-7005; 1791-7530

Carcinogenic molecules from cigarettes are known to cause DNA damage to bladder epithelial cells, but such damage can be corrected by some DNA repair mechanisms such as base and nucleotide excision repair, double-strand repair and mismatch repair. Various gene products play a role in these DNA repair systems. The aim of this study was to investigate six of these genes (XRCC1, XRCC3, XPD, XPG, APE1, hOGG1) each of which has a separate role in these repair mechanisms. The study was performed on 83 bladder cancer patients and 45 healthy controls. The genes were amplified by polymerase chain reaction (PCR) and restriction fragment polymorphism determinations were used to elucidate the specific changes in the gene region. There was no difference in smoking status between patient and control groups. It was found that there was a statistical significance in XRCC3 T carriers between patient and control groups and so there was a 4.87-fold protective role by the XRCC3 T allele against bladder cancer. The AA genotype and A allele carriers of the APE gene were more frequent in the transitional epithelial carcinoma group than in the adenocarcinoma group. The genotype distribution for the APE gene was determined to be significantly different between local and invasive cases; G allele carriers for this gene were significantly higher in invasive cancer types.