Interactions between pork consumption, CagA status and IL-1B-31 genotypes in gastric cancer

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).