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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