Mutagenesis vol. 18 no. 5 pp. 445-448,
September 2003
© 2003 UK Environmental Mutagen Society/Oxford University Press
DNA adducts in normal bladder tissue and bladder cancer risk
1INSERM and Evry University EMI 00-06, Statistical Methods and Genetic Epidemiology of Multifactorial Diseases, Evry, 2CNRS UPR2169, Genetic Instability and Cancer, Gustave-Roussy Institute, Villejuif, 3Department of Public Health, Gustave-Roussy Institute, Villejuif, 4Department of Urology, Mutualiste Montsouris Institute, Paris, 5Department of Urology, Necker Hospital, Paris, 6Department of Urology, Saint-Louis Hospital, Paris, 7INSERM U521, Gustave-Roussy Institute, Villejuif and 8Laboratory of Genotoxicity and Carcinogenesis, Curie Institute, Orsay, France
Cigarette smoking is an established cause of bladder cancer. The direct relationship between smoking-induced DNA adducts in bladder cells and cancer risk at that site has, however, been poorly assessed. We therefore investigated the relationship between bladder cancer risk and levels of DNA adducts measured in normal bladder biopsies by 32P-post-labeling in a hospital-based casecontrol study of 59 bladder cancer patients and 45 controls submitted to surgery for prostatic hyperplasia or urinary incontinence. An approximately 2-fold risk for bladder cancer was found in individuals with an adduct level >14.8 (median among controls) compared with those with an adduct level
14.8 (OR = 1.9, 95% CI 0.84.3, P = 0.13). A doseresponse relationship was also suggested (trend test, P = 0.13): compared with adduct levels below 13.5, the OR for bladder cancer was 1.7 (95% CI 0.64.6) for adduct levels between 13.5 and 18.5 and 2.2 (95% CI 0.86.1) for adduct levels >18.5. These findings provide some evidence that DNA adducts in bladder tissue might predict smoking-induced bladder cancer. Larger studies are still warranted to confirm these results.
9To whom correspondence should be addressed at: EMI 00-06, 523 Place des Terrasses de lAgora, 91034 Evry Cedex, France. Tel: +33 1 60 87 38 36; Fax: +33 1 60 87 38 48; Email: benhamou{at}evry.inserm.fr
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
D.-I. Kim, S.-J. Lee, S.-B. Lee, K. Park, W.-J. Kim, and S.-K. Moon Requirement for Ras/Raf/ERK pathway in naringin-induced G1-cell-cycle arrest via p21WAF1 expression Carcinogenesis, September 1, 2008; 29(9): 1701 - 1709. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Peters, G. Talaska, B. A.G. Jonsson, H. Kromhout, and R. Vermeulen Polycyclic Aromatic Hydrocarbon Exposure, Urinary Mutagenicity, and DNA Adducts in Rubber Manufacturing Workers Cancer Epidemiol. Biomarkers Prev., June 1, 2008; 17(6): 1452 - 1459. [Abstract] [Full Text] [PDF] |
||||
![]() |
F. L. Martin and K. T. Semple Environmental health impacts: occurrence, exposure and significance, Lancaster University, UK, 9-10 September 2003 Mutagenesis, September 1, 2004; 19(5): 423 - 429. [Abstract] [Full Text] [PDF] |
||||


