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IJE Advance Access published online on March 11, 2007
International Journal of Epidemiology, doi:10.1093/ije/dyl290
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Published by Oxford University Press on behalf of the International Epidemiological Association © The Author 2007; all rights reserved.

N-acetyltransferase phenotype and risk in urinary bladder cancer: approaches in molecular epidemiology. Preliminary results in Sweden and Denmark{dagger}

GM Lower, Jr1, T Nilsson2, CE Nelson2, H Wolf3, TE Gamsky1 and GT Bryan1

1Department of Human Oncology, University of Wisconin Center for Health Sciences, Madison, Wisconsin 53706, USA.
2Department of Urology, University Hospital, Lund, Sweden.
3Department of Urology, Hvidovre University Hospital, Copenhagen, Denmark.

The first 150 words of the full text of this article appear below.

A variable but often significant proportion of urinary bladder cancer in urban areas can be attributed to occupational and cultural (cigarette smoking) situations associated with exposures to various arylamines. The variable N-acetylation of carcinogenic arylamines by human hepatic enzyme systems, the known genetic regulation and polymorphic distribution of this enzyme activity in humans, and the known enhanced susceptibility of individuals with the genetically distinct ‘slow-acetylator’ phenotype to various arylamine toxicities, has prompted examination of possible correlations between N-acetyltransferase phenotype and urinary bladder cancer risk in rural and urban populations. In this context, N-acetylation is viewed as a component of detoxication pathways with respect to arylamine bladder carcinogenesis.

In preliminary utilizations of this approach, a population of urban urinary bladder cancer patients from Copenhagen, Denmark displayed a 13% excess (P = 0.065) of individuals with the slow acetylator phenotype (46/71 = 64.8%) when compared with a Danish . . . [Full Text of this Article]


   Introduction
 

   Methods
 
Patient and Control Populations
Clinical Methods

   Results
 

   Discussion
 

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