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	OR^a (95% CI)		AP (95% CI)
CYP1A12A × smoking^c
wt homozygote/no	65 : 136	1^d
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 × smoking^c
Present/no	31 : 91	1^d
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 × smoking^c
Present/no	59 : 129	1^d
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 × smoking^c
wt homozygote/no	52 : 103	1^d
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.