幽门螺杆菌、端粒酶基因和p53在胃癌及癌前病变中的表达及相关性研究

Study on the expression of hTERT,p53 and their relations in gastric cancers and precancerous lesions.

目的探讨幽门螺杆菌(Hp)、端粒酶基因(hTERT)、p53在胃癌及癌前病变中的表达及相关性。方法采用特殊染色、免疫组化和原位杂交方法,分别检测130例石蜡包埋标本中的Hp感染、p53蛋白和hTERT mRNA的表达。结果①在慢性浅表性胃炎、慢性萎缩性胃炎、非典型增生和胃癌患者中Hp的感染率分别为40%、60%、70%和72.5%。胃癌与慢性浅表性胃炎比较差异有统计学意义(P<0.05)。四种病变中p53蛋白的表达率分别为5%、25%、50%、62.5%,其中胃癌与慢性浅表性胃炎、慢性萎缩性胃炎比较差异有统计学意义(P<0.01)。hTERT mRNA的表达率分别为0、10%、30%、78.75%,胃癌与慢性萎缩性胃炎、非典型增生相比差异有统计学意义(P<0.05)。②Hp感染阳性的胃癌病例,p53、hTERT mRNA阳性的表达率明显高于Hp阴性胃癌病例(P<0.05);p53阳性的胃癌中端粒酶基因表达均为阳性,p53阴性的胃癌中有部分端粒酶基因表达阳性(66.7%)。结论Hp感染与p53基因的突变、hTERT活性密切相关;p53基因突变可导致端粒酶活化,但端粒酶激活可能不完全依赖于p53基因的调控。

Objective To study the expression of Hp,hTERT,p53 and their relations in gastric Cancer and precancerous lesions. Methods Special staining,immunohis to chemistry and in situ hybridization were used to detect Hp infection,the expression of p53 protein and hTERT mRNA in 130 cases of paraffin imbedding specimen of different gastric mucosal lesions. Results ①In chronic superficial gastritis （GSG）, chronic strophic gastritis （CAG） ,dysplasia（DYS） and gastric carcinoma （ GC ） ,the expression rates of Hp infection were 40% ,60% ,70%, and 72.5% respectively. There were significant differences between GC and CSG （P 〈 0.05 ）. The expression rates of p53 protein were 5% ,25% ,50% and 62.5% respectively; there were significant differences between GC and CAG,GC and CSG （ P 〈0.01 ）. The expression rates of hTERT mRNA were 0%, 10% ,30% and 78.75% respectively,there were significant differences between GC and CAG,GC and CSG,GC and DYS （ P 〈 0.05 ）. ②The p53, hTERT positive expression rate in gastric cancer was much higher in the Hp positive group than in the negative one （P 〈 0.05 ） ; The expression of hTERTmRNA was positive in all the p53 positive gastric cancer cases,while it was partly positive（ 66.7% ） in the p53 negative cases. Conclusion The mutation of p53 ,hTERT activation are closely associated with Hp infection; The mutation of p53 can induce the activation of telomerase, but the activation of telomerase does not depend on the p53 gene completely.