Abstract
The inflammatory process is known to increase the risk of gastric carcinogenesis, and both genetic and dietary factors are associated with inflammation. In the present study of 1,125 participants (373 cases and 752 controls), we determined whether the dietary inflammatory index (DII) is associated with the risk of gastric cancer (GC) and investigated whether a TNF polymorphism (rs1799964) modifies this association. Semi-quantitative food frequency questionnaire derived data were used to calculate the DII scores. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using multivariable logistic models adjusted for confounders. When we stratified the data by sex, the association between GC and the DII was significant only among the women (OR, 2.27; 95% CI 1.25–4.19), and the DII effect on the risk of GC differed depending on the TNF genotype (OR, 2.30; 95% CI 1.27–4.24 in TT genotype; OR, 0.78; 95% CI 0.37–1.65 in CC + CT, p for interaction = 0.035). Furthermore, the association between the DII and GC was significant in the Helicobacter pylori-positive group; similarly, the effect differed based on the TNF genotype (OR, 1.76; 95% CI 1.13–2.73 in TT genotype; OR,0.98; 95% CI 0.54–1.77 in CT + CC, p for interaction = 0.034). In conclusion, rs1799964 may modify the effect of the DII on GC.
Highlights
According to the GLOBOCAN results reported in 2018, gastric cancer (GC) is the fifth most common cancer worldwide, and the highest mortality rates are found in East Asia, including Korea[1]
The subjects with GC were more likely to be smokers and less likely to engage in regular exercise than the controls (p < 0.001 for all variables)
These variables might be associated with the GC risk and, were included in the subsequent statistical analyses that considered potential confounders
Summary
According to the GLOBOCAN results reported in 2018, gastric cancer (GC) is the fifth most common cancer worldwide, and the highest mortality rates are found in East Asia, including Korea[1]. The results of studies investigating the association between TNF genetic polymorphism and GC risk have been inconsistent[8,9]. These results indicate the need for further studies considering other factors, such as individual lifestyle factors. Environmental factors and host genetic factors contribute to the chronic inflammatory response Among these factors, dietary components contain both carcinogens and anticancer substances and are known to control the risk of c ancer[10]. The genetic sensitivity of the host can control the effects of the disease through complex interactions with environmental factors, and diets containing anticancer nutrients and carcinogens can modulate the risk of cancer development, especially in genetically vulnerable individuals[16,17]. We aimed to study whether differences in individual TNF genes have different effects on GC depending on eating habits and vice versa
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