Interleukin-8 polymorphisms are not associated with gastric cancer risk in a Polish population.

Inflammation seems to play a critical role in the development of many types of cancer, including gastric, colorectal, and bladder cancers (1-6). The presence of chronic inflammation has been well described in gastric cancer, the fourth most common cancer diagnosis and second most common cause of cancer death worldwide (4, 7-9). Genetic variants of several pathways critical for the inflammatory response have been studied and a number of single nucleotide polymorphisms (SNPs) in several genes from different pathways have been associated with gastric cancer risk, including IL1, IL1RN, IL1B, TNF, IL6, IL8 , and IL10 (10-17). Interleukin-8 (IL8), a potent chemokine, may play a role in gastric cancer pathogenesis. Gastric cancer specimens have increased IL-8 protein levels, and many gastric cancer cell lines express high levels of IL8 mRNA and protein (16, 18, 19). SNPs in the IL8 promoter ( 251 A>T, rs4073) and a linked SNP in intron 1 (IVS +230 G>T, rs2227307) were associated with increased risk for gastric cardia adenocarcinoma in a high-risk Chinese population (14). The A allele of the IL8 251 A>T SNP (rs4073) was associated with increased risk for gastric ulcer and gastric cancer in Helicobacter pylori –infected Japanese individuals (13). Increased IL-8 protein production was seen in individuals with the IL8 251 A allele after lipopolysaccharide stimulation of whole blood (20). The A allele also seems to increase transcriptional activity in vitro in response to IL1-1h and tumor necrosis factor-a stimulation (13). Central and Eastern European populations, including Poland, show a high incidence and mortality of stomach cancer among Caucasians (21). Because IL-8–mediated inflammation and IL8 SNPs may play a role in gastric cancer etiology, we studied genetic variation in IL8 in a populationbased case-control study of gastric cancer in individuals from Warsaw, Poland (22).