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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