RESUMO
Objective To investigate the expression of Ki-67,Survivin,Livin in dysplasia,colon carcinogenesis and para-carcinoma tissues,and to discuss the variation of cell proliferous capability in colon carcinogenesis and antiapoptosis factors.Methods 219 specimens were composed of mild,moderate and severe atypical hyperplasia,well,moderately,poorly differentiated adenocarcinoma,para-carcinoma tissues of 36,34,18,35,27,35 and 34 cases.Detected the expression of Ki-67,Survivin and Livin with tissue microarray and immunohistochemical methods.All data were statistically analyzed by SPSS 17.0.Results In mild,moderate and severe atypical hyperplasia,well,moderately,poorly differentiated adenocarcinoma and para-carcinoma tissues the expression of Ki-67 were (21.56 ± 19.20)％,(37.44 ± 17.41)％,(36.17 ± 17.41)％,(55.29 ± 16.13)％,(44.89 ± 29.67)％,(45.11 ± 29.24)％,(43.94 ± 28.84)％,Survivin were 13.8 ％,44.1％,77.8 ％,85.7 ％,85.1％,91.4 ％,91.1％,and Livin were 2.7 ％,38.2 ％,55.6 ％,100.0 ％,77.8 ％,80.8 ％,79.4 ％.The differences of Ki-67,Survivin and Livin expression in each group were statistically significant (F =6.796,X2 =81.754,X2 =95.200,all P ＜ 0.05).Ki-67 was significantly correlated with expression of Livin (r =0.360,P ＜ 0.05) and no correlated with expression of Survivin (r =0.044,P ＞ 0.05).Conclusion Colonic epithelium from mild atypical hyperplasia to proliferation of well-differentiated adenocarcinoma cells formed a peak,and gradually down to poorly differentiated adenocarcinoma formed a platform.When the colon epithelial cells to become cancerous,the capability of cell proliferation will significantly enhance,apoptosis inhibition will reach the peak and the tumor cell will happen the changes of malignant biological behavior.Tumor microenvironment may promote the cell proliferation in para-carcinoma tissues and the development of colon cancer.Livin may inhibit apoptosis and promot the progression in synergistic mechanism importing with Survivin,which play a role in the development of colonic adenocarcinoma.