B22

PURPOSE: This study aims to clarify the role of Helicobacter pylori(Hp) infection on the risk of digestive tract cancers, including oral squamous-cell carcinoma (SCC), esophageal SCC, gastric adenocarcinoma and colon adenocarcinoma.
 METHODS: One observational study and in vitro studies were conducted. For the observational study, 199 oral SCC, 317 esophageal SCC, 196 gastric adenocarcinoma and 240 colon adenocarcinoma patients were recruited for serum tests of Hp infection. Two hospital- and one community-based controls were used for the comparisons. Hp seropositivity was determined by an ELISA method against Hp IgG. In in vitro studies, one esophageal SCC (CE 81T/VGH) cell line was co-cultured with Hp, using one gastric adenocarcinoma (AGS) cell line as the control. Hp-induced cell apoptosis was determined by flow cytometry, TUNEL assay and Western immunoblotting to detect caspase-3 protein expressions in cell lysates.
 RESULTS: Presence of Hp infection was found to be inversely associated with esophageal SCC risk (adjusted odds ratio (AOR): 0.315-0.472; all p-value < 0.05) but positively associated with gastric adenocarcinoma (both cardia and non-cardia) (AOR: 1.636-3.060; all p-value < 0.05) in comparison to the three control groups. No associations were found in cancers of oral cavity and colon. In in vitro studies, increased apoptosis was found in CE 81T/VGH, but not in AGS cells, after being co-cultured with Hp at a concentration ratio of 1 Hp and 100 cancer cells for 36 hrs.
 CONCLUSION: An inverse association between Hp seropositivity and esophageal SCC risk was observed; its possible mechanism may be due to Hp-induced apoptosis in esophageal SCC cells.

Second AACR Centennial Conference on Translational Cancer Medicine-- July 20-23, 2008; Monterey, CA