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Stomach carcinogenesis progresses stepwise from normal mucosa/superficial gastritis, atrophic gastritis (GA) to gastric cancer (GC). Host factors independent of or combined withHelicobacter pyloriinfection may modulate the carcinogenesis process. In this two-stage study, we selected 24 putative functional tag single-nucleotide polymorphisms (tagSNPs) for sixH.pylori-related host genes,MUC1, toll-like receptor 4 (TLR4), protein tyrosine phosphatase, non-receptor type 11 (PTPN11),IL-1B,PGCandPGA3–5, and analyzed their influence and interaction withH.pylorion the GA and GC risks. Using high-throughput genotyping, the 24 tagSNPs were preliminarily assessed in a screening population of 552 controls, 254 GA and 236 GC subjects; subsequently, five candidate tagSNPs for gastric diseases risk in theTLR4,PGCandPTPN11genes were re-evaluated in a larger population of 1276 controls, 907GA and 714 GC subjects. We observed thatPGCrs6458238,PGCrs4711690 andPTPN11rs12229892 were associated with susceptibilities to GA and/or GC. Moreover, rs4711690 and rs12229892 andH.pyloridemonstrated significant interaction effects on GA risk. In gastric cancerous specimens, we observed significantly higher messenger RNA level in the subjects carrying thePGCrs6458238 GA genotype than that in subjects with the common GG genotype. These findings indicated that genetic variations of two crucialH.pylori-related host genes,H.pylori’s mucosal effecterPGCgene andH.pylori’scellular messengerPTPN11gene, either dependent or independent of interaction withH.pylori, were associated with the risks of GC and/or GA that precede carcinoma. Functional studies and further independent large-scale studies especially in other ethnic populations are still needed to confirm our results.

carcinogenesis

Helicobacter pylori              -related host gene polymorphisms associated with susceptibility of gastric carcinogenesis: a two-stage case-control study in Chinese