Objective:To investigate the correlation of typies of gastric intestinal metaplasia(IM),expression of p53,bcl-2 and the proliferating cell nuclear antigen(PCNA),with the lesion’s evolution. Methods:A total of 80 patients with IM(53 male and 27 female,35-64 years old) from an area with high-risk of gastric cancer(GC) in China were enrolled into this prospective study,including 28 cases of typeⅠ(complete),25 cases of typeⅡ(incomplete),and 27 cases of typeⅢ(incomplete).Of the 80 cases,62 cases including 19 cases of typeⅠ, 22 typeⅡand 21 typeⅢ,were followed up for 5-14 years(49 cases for 14 years,6 for 10 years,and 7 for 5 years).All of the 80 cases were studied immunohistochemically for the expression of p53,bcl-2 and PCNA. Results:The rate of p53-expressing cases was higher in typeⅢ(25.9%) than in typeⅠ(10.7%) and typeⅡ(12.0%),but without statistical significance(P=0.3070).The positive rate of bcl-2 was obviously lower in typeⅠ(21.4%) and typeⅡ(24.0%) than in typeⅢ(37.0%),but not statistically significant(P=0.4223).We observed difference in PCNA labelling index(LI) between typeⅡand typeⅢ(P=0.0037),and the difference was particularly significant in typeⅠas compared with typeⅢ(P<0.0001).There was no statistical significance between typeⅠand typeⅡ(P=0.0616). Evolution into GC was detected in 0%,4.5%,and 14.3%of typeⅠ,typeⅡ,and typeⅢIM cases,respectively. Progression to dysplasia was detected in 31.6%,18.2%,and 14.3%of typeⅠ,typeⅡ,and typeⅢIM cases, respectively.Persistence of IM was documented in 31.6%,45.5%,and 42.9%of typeⅠ,typeⅡ,and typeⅢIM cases, respectively.Regression of IM was documented in 36.8%,31.8%,and 28.6%of typeⅠ,typeⅡ,and typeⅢIM cases, respectively. In progressive,persistent and regressive groups,the positive rates of p53 were 17.6%,16.0%and 15.0%,bcl-2 were 29.4%,36.0%and 25.0%,and PCNA LIs were 24.953±14.477,23.752±12.934 and 25.105±10.055,respectively. There were no significant differences between the groups. Conclusion:The present follow-up study indicated that typeⅢhad a higher risk for development of cancer than typeⅠorⅡ.PCNA LI was significantly higher in typeⅢthan in typeⅠandⅡ,suggesting that cell proliferation in typeⅢwas more active.Our data also indicated that the expression of p53 and bcl-2 had no apparent association with the particular type and the expression of p53,bcl-2 and PCNA had no apparent correlation with evolution of IM.Further studies with a larger sample size are needed to verify present observation. Objective: To investigate the correlation of typies of gastric intestinal metaplasia (IM), expression of p53, bcl-2 and the proliferating cell nuclear antigen (PCNA), with the lesion’s evolution. Methods: A total of 80 patients with IM and 27 female, 35-64 years old) from an area with high-risk of gastric cancer (GC) in China were enrolled into this prospective study, including 28 cases of type I (complete), 25 cases of type II Of the 18 cases of type III (incomplete). Of the 80 cases, 62 cases including 19 cases of type I, 22 type II and 21 type III, were followed up for 5-14 years (49 cases for 14 years, 6 for 10 years, and 7 for 5 years). All of the 80 cases were studied immunohistochemically for the expression of p53, bcl-2 and PCNA. Results: The rate of p53-expressing cases was higher in type III (25.9%) than in type I (10.7%) and type II 12.0%), but without statistical significance (P = 0.3070). The positive rate of bcl-2 was obviously lower in type Ⅰ (21.4%) and type Ⅱ (P = 0.0037), and the difference was particularly significant in type I compared with type III (P <0.0001), but not statistically significant (P = 0.4223) .We observed difference in PCNA labelling index . There was no statistical significance between type I and type II (P = 0.0616). Evolution into GC was detected in 0%, 4.5%, and 14.3% of type I, type II, and type III IM cases, respectively. Progression to dysplasia was detected in 31.6% 18.2%, and 14.3% of type I, type II, and type III IM cases, respectively. Persistence of IM was documented in 31.6%, 45.5%, and 42.9% of type I, type II, and type III IM cases, respectively. In progressive, persistent and regressive groups, the positive rates of p53 were 17.6%, 16.0% and 15.0%, respectively, and bcl-2 were 29.4%, 36.0%, 31.8%, and 28.6% % and 25.0%, and PCNA LIs were 24.953 ± 14.477, 23.752 ± 12.934 and 25.105 ± 10.055, respectively. There were no significant differences between the groups. Conclusion: The present follow-up study indicated that typeⅢhad a higher risk for development of cancer than typeⅠorⅡ.PCNA LI was significantly higher in typeⅢthan in typeⅠandⅡ, suggesting that cell proliferation in type Ⅲ was more active. Our data also indicates that the expression of p53 and bcl-2 had no apparent association with the particular type and the expression of p53, bcl-2 and PCNA had no apparent correlation with evolution of IM. Future studies with a larger sample size are needed to verify present observation.