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AIM: To investigate the effect of -Helicobacter pylori(H pylori)in fection on the expressions of Bcl-2 family members ingastric adenocarcinoma.METHODS: Gastric adenocarcinoma and resection margin tissues of 95 patients were studied. Semi-quantitative RT-PCR was used to measure Bid, Bax and Bcl-2 mRNA expressions.RESULTS: Expressions of Bid and Bax in gastric adenocarcinoma tissues without -Hpyloriinfection, with cagA-Hpyloriinfection and cagA+ Hpyloriinfection increased significantly in t (Bid, 0.304, 0.422 and 0.855 respectively, P＜0.05; Bax,0.309, 0.650 and 0.979 respectively, P＜0.05). Bcl-2 mRNA levels increased significantly in gastric adenocarcinoma tissues with cagA- H pyloriinfection and cagA+ H pylori infection, compared with those without H pylori infection(0.696 and 0.849 vs0.411, P＜0.05). Expressions of Bid,Bax and Bcl-2 in resection margin tissues without H pyloriinfection, with cagA- H pyloriinfection and cagA+ H pylori infection increased significantly in t (Bid, 0.377, 0.686 and 0.939 respectively, P＜0.05; Bax, 0.353, 0.645 and 1.001 respectively, P＜0.05; Bel-2, 0.371, 0.487 and 0.619respectively, P＜0.05). In H pylori negative specimens,expressions of Bid and Bax correlated negatively with that of Bcl-2 respectively in adenocarcinoma tissues (Bid vs Bcl-2, r=-0.409, P＜0.05; Bax vs Bcl-2, r=-0.451, P＜0.05). In H pylori positive specimens, expressions of Bid and Bax did not correlate with that of Bcl-2 in adenocarcinoma tissues (Bid vs Bcl-2, r=0.187, P＞0.05; Bax vs Bcl-2, r=0.201,P＞ 0.05), but correlated positively with that of Bcl-2 respectively in resection margin tissues (Bid vs Bcl-2, r=0.331, P＜0.05;Bax vsBcl-2, r=-0.295, P＜0.05).CONCLUSION: H pylori may enhance Bid, Bax and Bcl-2 mRNA levels and cause deregulation of these apoptosis-associated genes expressions, which may play a role during development of gastric adenocarcinoma induced by H pylori.