Bladder cancer and polymorphisms of DNA repair genes (XRCC1, XRCC3, XPD, XPG, APE1, hOGG1).
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.
Istanbul Universitesi Deneysel Tip Arastirma Enstitüsü, Molekuler Tip Anabilim Dali, Capa, Istanbul, Turkey.
Kamil Fehmi
KF
Narter
Arzu
A
Ergen
Bedia
B
Agaçhan
Uzay
U
Görmüs
Ozlem
O
Timirci
Turgay
T
Isbir
D000230:Adenocarcinoma / Q000235:genetics* / Q000556:secondary; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002295:Carcinoma, Transitional Cell / Q000235:genetics* / Q000556:secondary; D016022:Case-Control Studies; D045647:DNA Glycosylases / Q000235:genetics; D004260:DNA Repair; D045643:DNA Repair Enzymes / Q000235:genetics*; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics; D004720:Endonucleases / Q000235:genetics; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009687:Nuclear Proteins / Q000235:genetics; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic / Q000235:genetics*; D012150:Polymorphism, Restriction Fragment Length; D014157:Transcription Factors / Q000235:genetics; D001749:Urinary Bladder Neoplasms / Q000235:genetics* / Q000473:pathology; D000076105:X-ray Repair Cross Complementing Protein 1; D051759:Xeroderma Pigmentosum Group D Protein / Q000235:genetics; D000099250:DNA Excision Repair Protein ERCC-5
D045647:DNA Glycosylases; D045643:DNA Repair Enzymes; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase; D004268:DNA-Binding Proteins; D004720:Endonucleases; D009687:Nuclear Proteins; D014157:Transcription Factors; D000076105:X-ray Repair Cross Complementing Protein 1; D051759:Xeroderma Pigmentosum Group D Protein; D000099250:DNA Excision Repair Protein ERCC-5; C110901:X-ray repair cross complementing protein 3; C000619371:XRCC1 protein, human; C479058:oxoguanine glycosylase 1, human; C085108:APEX1 protein, human; C497292:ERCC2 protein, human