P-0034 An Exacerbated Pro-Inflammatory State may Increase the Risk of H. Pylori-Associated Gastric Cancer Development

Abstract Introduction Helicobacter pylori infects the majority of the adult population worldwide and results in gastric cancer development in about one percent of the infected patients. The multifactorial etiology of gastric cancer includes the interaction between inflammatory (pro-tumor) and anti-inflammatory (anti-tumor) cytokines. In this study we aimed to evaluate the level of some of these cytokines in Iranian gastric cancer patients. Methods Fasting blood samples were collected from 93 gastric cancer and 97 cancer-free subjects. The histologic subtype of every tumor patients was intestinal in the two subsites of cardia (N=39) and non cardia (N=54). Serum samples were analyzed for IL-6, IL-7, IL-8, IL-10 and TNF-alpha using Milliplex®MAP High sensitivity human cytokine magnetic bead panel immunoassay. Statistical analyses were performed using SPSS version 11.5 software. Comparisons between each two groups were performed using Mann-Whitney U test. Differences were considered significant when P values were equal or below 0.05. Results Mean serum values for IL-6, IL-8 and IL-10 levels were respectively 16, 2 and 9 fold greater in intestinal type gastric cancer patients versus controls (P Conclusion Increasing evidence is supporting the etiologic role of immune regulatory state in gastric cancer development. Our data support the fact that a shifted balance toward pro-inflammatory (IL-6, IL-8) versus anti-inflammatory (IL-10) state may increase the chances of intestinal type gastric cancer development in both cardia and noncardia subsites.