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Carcinogenesis Advance Access published online on August 19, 2004
Carcinogenesis, doi:10.1093/carcin/bgh251
© 2004 by Oxford University Press
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Received April 19, 2004
Revised June 30, 2004
Accepted July 25, 2004

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Genetic polymorphisms in UDP-glucuronosyltransferases and glutathione S-transferases and colorectal cancer risk

E. M. J. van der Logt 1, S. M. Bergevoet 1, H. M. J. Roelofs 1, Z. van Hooijdonk 1, R. H. M. te Morsche 1, T. Wobbes 2, J. B. de Kok 3, F. M. Nagengast 1, W. H. M. Peters 1*

1 Department of Gastroenterology, University Medical Centre St Radboud, Nijmegen, The Netherlands
2 Department of Surgery, University Medical Centre St Radboud, Nijmegen, The Netherlands
3 Department of Clinical Chemistry, University Medical Centre St Radboud, Nijmegen, The Netherlands

* To whom correspondence should be addressed. E-mail: w.peters{at}mdl.umcn.nl.


  Abstract

Colorectal cancer (CRC) is one of the most common malignancies in the Western world showing an increasing incidence, and has been associated with genetic and lifestyle factors. Individual susceptibility to CRC may be partly due to variations in detoxification capacity in the gastrointestinal tract. Genetic polymorphisms in detoxification enzymes may result in variations in detoxification activities, which subsequently might influence the levels of toxic/carcinogenic compounds, and this may influence the risk for CRC. To determine whether genetic polymorphisms in detoxification enzymes predispose to the development of CRC, 371 patients with sporadic CRC and 415 healthy controls were genotyped for polymorphisms in the important detoxification enzymes UDP-glucuronosyltransferase UGT1A1, UGT1A6, UGT1A7 and UGT1A8, and glutathione S-transferase GSTA1, GSTM1, GSTP1 and GSTT1. Patients and controls were all of Caucasian origin. DNA was isolated from either blood or tissue and tested by polymerase chain reaction followed by restriction fragment length polymorphism analyses. Logistic regression analyses showed significant ageand gender-adjusted risks for CRC associated with variant genotypes of UGT1A6 (OR 1.5, 95% CI 1.03-2.3) and UGT1A7 (OR 2.4, 95% CI 1.3-4.6), whereas no associations were found between CRC and the other polymorphic genes as mentioned above. In conclusion, these data suggest that the presence of variant UGT1A6 and UGT1A7 genotypes with expected reduced enzyme activities, might enhance susceptibility to CRC.


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