The Effect of CYP, GST, and SULT Polymorphisms and Their Interaction with Smoking on the Risk of Hepatocellular Carcinoma
Table 4
Effect of the gene-smoking interaction on the development of hepatocellular carcinoma.
Cases : controls
ORa (95% CI)
AP (95% CI)
CYP1A12A × smokingc
wt homozygote/no
65 : 136
1d
wt homozygote/yes
98 : 90
2.16 (1.29–3.36)
mt carrier/no
20 : 37
1.08 (0.58–2.03)
mt carrier/yes
35 : 27
2.81 (1.51–5.23)
0.680
0.201 (−0.328; 0.730)
GSTM1 × smokingc
Present/no
31 : 91
1d
Present/yes
62 : 48
4.01 (2.20–7.28)
Null/no
48 : 81
1.82 (1.05–3.18)
Null/yes
57 : 69
2.34 (1.32–4.23)
0.004
nc
GSTT1 × smokingc
Present/no
59 : 129
1d
Present/yes
81 : 91
1.86 (1.17–2.97)
Null/no
20 : 43
0.99 (0.53–1.86)
Null/yes
38 : 26
3.13 (1.69–5.82)
0.230
0.480 (0.001; 0.815)
SULT1A1 × smokingc
wt homozygote/no
52 : 103
1d
wt homozygote/yes
78 : 77
1.93 (1.19–3.14)
mt carrier/no
33 : 70
1.01 (0.59–1.75)
mt carrier/yes
55 : 40
3.05 (1.73–5.40)
0.250
0.363 (−0.021; 0.747)
OR: odds ratio; CI: confidence interval; AP: attributable proportion; nc: not calculable.
aAdjusted for age and sex. from test for multiplicative interaction.
cThe sum does not add up to the total because of some missing values.
dReference category. wt: wild-type allele. mt: variant-type allele.