Consequently, we examined the association of NAT1*10 with prostate cancer risk, grade, and stage among 400 Finnish male smokers using a case-control study design.
The meta-analysis included six studies with NAT1 genotyping (610 prostate cancer cases and 713 controls), and 10 studies with NAT2 genotyping (1,253 cases and 1,722 controls).
A high intake of well-done meat and the presence of the rapid NAT1 and slow NAT2 acetylator genotypes, as modifiers of the carcinogenic effect of heterocyclic amines, were hypothesized to increase PC risk and possibly explain these ethnic differences in risk.
There was no association between PCa and either 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) intake, or NAT1 and NAT2 genotypes.
The results of this small pilot study suggest increased susceptibility to prostate cancer for subjects with combinations of NAT1*10 and slow (particularly very slow) NAT2 acetylator genotypes.
When the NAT1*10 heterozygote and other genotypes without NAT1*10 allele were considered as low risk genotypes, NAT1*10/NAT1*10 had a significantly higher risk of PCa (OR = 2.4, 95% CI; 1.0-5.6).