Cancer Causes & Control

, Volume 14, Issue 3, pp 293–298

Rapid N-acetyltransferase 2 imputed phenotype and smoking may increase risk of colorectal cancer in women (Netherlands)

Authors

  • Olga L. van der Hel
    • Julius Center for Health Sciences and Primary CareUniversity Medical Centre, Utrecht
  • H. Bas Bueno de Mesquita
    • Department of Chronic Diseases EpidemiologyNational Institute of Public Health and the Environment, Bilthoven
  • Lodewijk Sandkuijl
    • Julius Center for Health Sciences and Primary CareUniversity Medical Centre, Utrecht
  • Paul A.H. van Noord
    • Julius Center for Health Sciences and Primary CareUniversity Medical Centre, Utrecht
  • Peter L. Pearson
    • Department of Medical GeneticsUniversity Medical Centre, Utrecht
  • Diederick E. Grobbee
    • Julius Center for Health Sciences and Primary CareUniversity Medical Centre, Utrecht
  • Petra H.M. Peeters
    • Julius Center for Health Sciences and Primary CareUniversity Medical Centre, Utrecht
Article

DOI: 10.1023/A:1023601922106

Cite this article as:
van der Hel, O.L., Bas Bueno de Mesquita, H., Sandkuijl, L. et al. Cancer Causes Control (2003) 14: 293. doi:10.1023/A:1023601922106

Abstract

Objective: The relationship between smoking and colorectal cancer risk and whether such effect is modified by variations in the NAT2 genotype is investigated. Methods: In the prospective DOM (Diagnostisch Onderzoek Mammacarcinoom; 27,722 women) cohort follow-up from 1976 until 1987 revealed 54 deaths due to colon or rectal cancer, and follow-up from 1987 to 01-01-1996 revealed 204 incident colorectal cancer cases. A random sample (n = 857) from the baseline cohort was used as controls. Four NAT2 restriction fragment length polymorphisms (RFLPs) were analysed using DNA extracted from urine samples. Rapid or slow acetylator phenotype status was attributed to individuals. Results: Smoking may increase the risk for colon cancer (RR = 1.36, 95% CI 0.97–1.92) as well as for rectal cancer (RR = 1.31, 95% CI 0.76–2.25), although not statistically significant. Rapid NAT2 acetylation did not increase colorectal cancer risk, but in combination with smoking the risk was statistically significant increased, compared to women who had a slow NAT2 imputed phenotype and never smoked (RR = 1.56, 95% CI 1.03–2.37). For colon cancer, but not for rectal cancer the increased risk was statistically significant (RR = 1.67, 95% CI, 1.05–2.67 versus RR = 1.30 95% CI 0.63–2.68). Conclusions: Our study points to smoking as a risk factor for colon and rectal cancer and, in addition, especially in women with rapid NAT2 imputed phenotype.

colorectal cancerN-acetyltransferase 2prospective studysmokingwomen
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Copyright information

© Kluwer Academic Publishers 2003