Skip to main content

Table 2 Odds Ratios (95% CI) of gastric cancer for SNPs in metabolic genes and their frequency distribution among 107 cases and 254 controls

From: Polymorphisms in metabolic genes, their combination and interaction with tobacco smoke and alcohol consumption and risk of gastric cancer: a case-control study in an Italian population

  

Cases % (n)

Controls % (n)

OR (95% CI) * †

GSTM1 null

 

56.2 (59)

52.7 (135)

1.13 (0.71–1.79)

GSTT1 null

 

37.1 (39)

22.4 (57)

2.10 (1.27–3.44)

CYP1A1*2A

 

20.5 (22)

22.0 (56)

0.88 (0.50–1.54)

CYP2E1*5

 

4.7 (5)

7.8 (20)

0.54 (0.20–1.50)

CYP2E1*5A or *6

 

14.5 (15)

10.6 (27)

1.33 (0.67–2.65)

NAT2 Slow ‡

 

59.8 (64)

51.8 (131)

1. 38 (0.88–2.19)

SULT1A1

Arg/His

36.5 (39)

33.5 (85)

1.35 (0.82–2.21)

 

His/His

10.3 (11)

5.1 (13)

2.46 (1.03–5.90)

EPHX1 exon 3

Tyr/His

38.7 (41)

36.0 (90)

1.24 (0.76–2.04)

 

His/His

14.1 (15)

11.2 (28)

1.37 (0.67–2.80)

EPHX4 exon 4

His/Arg

30.5 (32)

37.4 (95)

0.77 (0.47–1.27)

 

Arg/Arg

5.7 (6)

2.4 (6)

2.28 (0.70–7.20)

Imputed mEH phenotypes ^

Rapid

15.8 (15)

23.7 (59)

0.60 (0.30–1.15)

 

Slow

25.3 (24)

21.2 (54)

1.00 (0.55–1.78)

 

Very slow

8.4 (8)

8.6 (21)

0.82 (0.33–2.00)

  1. * OR adjusted for age and gender
  2. † Reference groups are the homozygous wild genotypes for each gene
  3. ‡ Reference group is fast acetylators (homo-heterozygous for the wild-type allele)
  4. ^ Reference group is the normal imputed phenotype