Table SB.
Combined effects of N-acetyltransferase polymorphisms and cigarette smoking on PCa risk.
| N-acetyltransferase status | Unadjusted OR (95% CI)a #Cases||#Ctrlsc |
Adjusted OR (95% CI)b | ||
|---|---|---|---|---|
|
|
|
|||
| Non-smokers | Ever-smokers | Non-smokers | Ever-smokers | |
| NAT2 Rapid alleles | 1.00 (Reference) 5||5 |
2.04 (0.54–7.62) 57||28 |
1.00 (Reference) | 1.46 (0.33–6.45) |
| ≥1 NAT2 Slow allele(s) | 0.71 (0.13–3.87) 5||7 |
3.19 (0.84–12.10) 67||21 |
0.33 (0.05–2.24) | 2.06 (0.45– 9.42) |
| P-value for interaction | 0.1445 | |||
Notes:
a
Associations were determined using multivariate logistic regression models to estimate the risk of developing PCa using Inheritance of two NAT2 rapid alleles and non-smokers as the referent category;
b
Risk estimates adjusted for age and West African Ancestry, modeled as continuous variables;
c
The analysis was restricted to study participants who had available smoking and N-acetyltransferase genotype status analysis.