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Table 5 Prostate cancer risk and HAA intake stratified by NAT2-imputed phenotype and CYP1A1 and CYP1A2 genotype

From: Association between NAT2, CYP1A1, and CYP1A2 genotypes, heterocyclic aromatic amines, and prostate cancer risk: a case control study in Japan

  HAA intake  
Low Moderate High P interaction
NAT2-imputed phenotype
 Rapid or intermediate acetylator     
 Cases/Controls 92/124 100/116 132/93  
 OR (95% CI)a 1.00 1.17 (0.84–1.65) 1.85 (1.34–2.56)  
 Slow acetylator     
 Cases/Controls 8/7 8/8 11/3  
 OR (95% CI) 1.43 (0.50–4.12) 1.21 (0.56–2.60) 5.29 (2.37–11.80) 0.004
CYP1A1
 AA     
  Cases/controls 51/87 68/82 88/63  
  OR (95% CI) 1.00 1.46 (0.95–2.24) 2.41 (1.61–3.63)  
 GA + GG     
  Cases/controls 49/44 40/42 55/33  
  OR (95% CI) 2.05 (1.19–3.63) 1.72 (1.07–2.76) 2.86 (1.83–4.47) < 0.001
CYP1A2
 CC     
  Cases/controls 7/17 14/17 13/13  
  OR (95% CI) 1.00 2.05 (0.73–5.77) 2.65 (0.97–7.29)  
 CA + AA     
  Cases/controls 93/114 94/107 130/83  
 OR (95% CI) 2.17 (0.85–5.59) 2.34 (0.93–5.92) 4.01 (1.60–10.05) 0.003
  1. BMI body mass index, OR odds ratio, CI confidence interval, HAA heterocyclic aromatic amine
  2. aOR (95% CI) adjusted by conditional logistic regression for alcohol intake, smoking status, BMI, family history of prostate cancer, and total energy intake