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. 2014 Jul 7;20(25):8151–8157. doi: 10.3748/wjg.v20.i25.8151

Table 2.

Joint effects of pork consumption, CagA status and interleukin-1B-31 genotypes on the risk of gastric cancer1

Genotype of IL-1B-31 Pork consumption
Low (< 25 g/d)
High (≥ 25 g/d)
Hp CagA (-)
Hp CagA (+)
Hp CagA (-)
Hp CagA (+)
Case/control OR Case/control OR Case/control OR Case/control OR
TT 9/15 1.00 16/15 1.00 11/30 1.00 5/29 1.00
TC 11/58 0.42 (0.14-1.11) 30/39 0.71 (0.31-1.98) 20/49 1.25 (0.47-2.81) 23/34 2.98 (0.99-11.30)
CC 12/27 0.71 (0.27-2.36) 11/23 0.46 (0.16-1.54) 27/25 0.86 (0.29-2.35) 16/23 3.11 (1.08-12.66)
C carrier 23/85 0.45 (0.18-1.37) 41/62 0.69 (0.33-1.63) 27/74 1.00 (0.48-2.06) 39/57 3.07 (1.17-10.79)

1Adjusted for the following confounding factors: age, gender, education, smoking, alcohol, and family history. P for multiplicative interaction: Pork consumption and Helicobacter pylori (H. pylori) CagA status: 0.11 [adjusted by age, gender, education, smoking, alcohol, family history and interleukin (IL)-1B-31 C carrier]; Pork consumption and IL-1B-31 C carrier: 0.048 (adjusted by age, gender, education, smoking, alcohol, family history and H. pylori CagA status).