ABSTRACT
Objective To investigate the expression of pro-apoptotic factor (Smac) and Survivin in gastric ulcer tissue.Methods Selected the 80 cases of gastric ulcer patients as the research object in the first people′s hospital of neijiang,in which no precancerous lesions of 40 cases of gastric ulcer (N group),40 cases of precancerous lesions of gastric ulcer(Y group),two groups of patients were Smac mRNA and Survivin mRNA were detected by using PCR method,immunohistochemical SP method of Smac and Survivin in specimens of table detect.Gastric ulcer patients were treated by triple therapy,and the apoptosis index was detected by TUNEL.Results Smac in N group(++) and (+++) in the expression accounted for 82.5％ was higher than that in Y group accounted for 47.5％,Survivin in group N (++) and (+++) in the expression accounted for 15.0％ was significantly lower than Y group accounted for 35.0％;And Smac mRNA in the N group relative expression the amount was significantly higher than that of Y group,while the expression of Survivin mRNA in the N group were significantly lower than Y group;N group the apoptosis index of the triple therapy after treatment than before treatment significantly decreased,the difference was statistically significant(P<0.05).Conclusion The clinical application of Smac and Survivin can be used as an auxiliary diagnostic index for the diagnosis of precancerous lesions in patients with gastric ulcer.Patients with gastric ulcer without precancerous lesion treated by triple therapy which can effectively control the apoptosis index of patients,improve the survival rate of patients.
ABSTRACT
MDR(multidrug-resistance)is a major obstacle in the chemotherapy of cancer.Numerous mechanisms are known to contribute to MDR,alterations at the level of apoptosis control are one of those mechanisms except overexpression of drug efflux pumps.This review focuses on the research progression of alterations at the level of apoptosis inducing MDR,and some of the strategies that have been used in an attempt to chemosensitize resistant tumors by manipulating dysregulated apoptosis pathways.