The Role Of P33～(ING1),Survivin And Ki67 Protein In Carcinogenesis And Development Of Esophageal Carcinoma

Objective: It is necessary for the balance of the Proliferation and apoptosis to stabilize cell amounts and eliminate aberrant cells in case of carcinogenesis. The proliferation, differentiation and apoptosis of normal cells are strictly controlled by a lot of genes and balance disorders among these factors are closely correlated with the carcinogenesis and development of cancers. As many cancers, the carcinogenesis and development of esophageal carcinoma not only involves activation of proto-oncogene and inhibition of antioncogene, but also involves cell proliferation and apoptosis factors. In this study, immunohistochemical technique were used to investigate the expressions P33^ING1,Survivin and Ki67 in different epithelial lesions, including normal, hyperplasia, displasia and invasive carcinoma and to analyze the expressions P33^ING1,Survivin and Ki67 correlated with pathologic characteristics. Methods: Immunohistochemistry was used to detect the expressions of P33^ING1,Survivin and Ki67 in 51 cases of whole specimen of esophageal carcinoma with different degree epithelial lesions .Results :The expressions of P33^ING1 was reducing and those of Survivin and Ki67 were progressively increasing in the course from normal epithelia. simple hyperplasia and dysplasia to invasive carcinoma; Significant differences were observed in the expressions of P33^ING1,Survivin and Ki67 between normal and displasia, invasive carcinoma(p<0.01); The expression of P33^ING1 was negatively related to the depth of invasion and was positively related to the infiltration depth(G1, G3)in the esophageal carcinomas(P<0.05); The expression of P33^ING1 in esophageal invasive carcinoma was negatively relationship correlated with those of Survivin and Ki67(P<0.01).Conclusion: The expression of P33^ING1 decrease gradually from normal epithelia, simple hyperplasia and dysplasia to invasive carcinoma ,and can be a histology sign the predictive warning of esophageal carcinoma. The expression of Survivin and Ki67go up from normal epithelia, simple hyperplasia and dysplasia to invasive carcinoma. No significant difference was observed for the expression of Surviving and Ki67 between severe dysplasia and carcinoma. Severe dysplasia has the character of cancerous; The high expression of Ki67 in dysplasia shows proliferation of cells increase and it is connected with the developing of the esophageal carcinoma; Survivin expression has positive correlation with Ki67, but has negative correlation with P33^ING1 in dysplasia and esophageal carcinoma. Combined detection of the expression of P33^ING1, Survivin and Ki67 are useful for the diagnosing the esophageal carcinoma precancerous lesion. The activation of Survivin gene, enhancement of Ki67 function and down-regulation of P33^ING1 function combined to resist cell apoptosis and contributed to the carcinogenesis and development of esophageal carcinoma. They could probably provide some useful ways on early diagnosis, therapy and prognostic analysis for esophageal carcinomas.