AIM: To examine the interactions between cytotoxinassociated gene (CagA) positive Helicobacter pylori infection and smoking in non-cardiac gastric cancer.METHODS: A case-control study (257 cases and 514 frequency-matc...AIM: To examine the interactions between cytotoxinassociated gene (CagA) positive Helicobacter pylori infection and smoking in non-cardiac gastric cancer.METHODS: A case-control study (257 cases and 514 frequency-matched controls) was conducted from September 2008 to July 2010 in Xi’an,China.Cases were newly diagnosed,histologically confirmed non-cardiac cancer.Controls were randomly selected from similar communities to the cases and were further matched by sex and age (± 5 years).A face-to-face interview was performed by the investigators for each participant.Data were obtained using a standardized questionnaire that included questions regarding known or suspected lifestyle and environmental risk factors of gastric cancer.A 5 mL sample of fasting venous blood was taken.CagA infection was serologically detected by enzymelinked immunosorbent assays.RESULTS: Smoking and CagA infection were statistically significant risk factors of non-cardiac cancer.CagA was categorized in tertiles,and the odds ratio (OR) was 12.4 (95% CI: 6.1-20.3,P = 0.003) for CagA after being adjusted for confounding factors when the highexposure category was compared with the low-exposure category.Smokers had an OR of 5.4 compared with subjects who never smoked (95% CI: 2.3-9.0,P = 0.002).The OR of non-cardiac cancer was 3.5 (95% CI: 1.8-5.3) for non-smokers with CagA infection,3.5 (95% CI: 1.9-5.1) for smokers without CagA infection,and 8.7 (95% CI: 5.1-11.9) for smokers with CagA infection compared with subjects without these risk factors.After adjusting for confounding factors,the corresponding ORs of non-cardiac cancer were 3.2 (95% CI: 1.5-6.8),2.7 (95% CI: 1.3-4.9) and 19.5 (95% CI: 10.3-42.2),respectively.There was a multiplicative interaction between smoking and CagA,with a synergistic factor of 2.257 (Z = 2.315,P = 0.021).CONCLUSION: These findings support a meaningful interaction between CagA and smoking for the risk of gastric cancer which may have implications for its early detection.展开更多
基金Supported by Health department of Shaanxi Province,China,No.2009K12-022
文摘AIM: To examine the interactions between cytotoxinassociated gene (CagA) positive Helicobacter pylori infection and smoking in non-cardiac gastric cancer.METHODS: A case-control study (257 cases and 514 frequency-matched controls) was conducted from September 2008 to July 2010 in Xi’an,China.Cases were newly diagnosed,histologically confirmed non-cardiac cancer.Controls were randomly selected from similar communities to the cases and were further matched by sex and age (± 5 years).A face-to-face interview was performed by the investigators for each participant.Data were obtained using a standardized questionnaire that included questions regarding known or suspected lifestyle and environmental risk factors of gastric cancer.A 5 mL sample of fasting venous blood was taken.CagA infection was serologically detected by enzymelinked immunosorbent assays.RESULTS: Smoking and CagA infection were statistically significant risk factors of non-cardiac cancer.CagA was categorized in tertiles,and the odds ratio (OR) was 12.4 (95% CI: 6.1-20.3,P = 0.003) for CagA after being adjusted for confounding factors when the highexposure category was compared with the low-exposure category.Smokers had an OR of 5.4 compared with subjects who never smoked (95% CI: 2.3-9.0,P = 0.002).The OR of non-cardiac cancer was 3.5 (95% CI: 1.8-5.3) for non-smokers with CagA infection,3.5 (95% CI: 1.9-5.1) for smokers without CagA infection,and 8.7 (95% CI: 5.1-11.9) for smokers with CagA infection compared with subjects without these risk factors.After adjusting for confounding factors,the corresponding ORs of non-cardiac cancer were 3.2 (95% CI: 1.5-6.8),2.7 (95% CI: 1.3-4.9) and 19.5 (95% CI: 10.3-42.2),respectively.There was a multiplicative interaction between smoking and CagA,with a synergistic factor of 2.257 (Z = 2.315,P = 0.021).CONCLUSION: These findings support a meaningful interaction between CagA and smoking for the risk of gastric cancer which may have implications for its early detection.
