CD133、β-catenin和hTERT在胃癌及癌前病变中的表达及相关性研究

摘要

目的 探究CD133、β-catenin和人端粒酶逆转录酶(human telomerase reverse transcriptase, hTERT)在胃癌及癌前病变中表达的临床意义及其相关性.方法 收集上海市静安区市北医院收治的60例胃癌标本、60例癌前病变标本和40例胃炎标本,采用免疫组化法检测CD133、β-catenin和hTERT蛋白的表达情况,探究CD133、β-catenin和hTERT表达水平与临床病理因素的关系,分析三者之间的相关性.结果 在胃癌组织和癌前病变组织中,CD133、β-catenin和hTERT表达水平明显增加,与胃炎组织相比,CD133、β-catenin和hTERT在胃癌和癌前病变组织中的表达差异有统计学意义(P<0.01).与癌前病变组织相比,以上三种蛋白在胃癌组织中表达显著上调,差异有统计学意义(P<0.01).在癌前病变组织中,CD133、β-catenin和hTERT的表达与患者的临床病理因素均无相关性,而在胃癌患者中,三者的表达与淋巴结转移、分化程度和浸润深度有关(P< 0.05).另外,在胃癌中CD133、β-catenin和hTERT两两之间均呈正相关(P<0.05).结论 CD133、β-catenin和hTERT的协同高表达与胃癌的发生及癌前病变向胃癌的发展密切相关,其可能成为抑制癌前病变向胃癌转化的关键因子.%Objective To investigate the clinical significance and correlation of CD133, β-catenin and human telomerase reverse transcriptase (hTERT) in gastric cancer and precancerous lesion.Methods Sixty cases of gastric cancer specimens, 60 cases of precancerous lesions and 40 cases of gastritis specimens were collected in Jing'an District Shibei Hospital.The expressions of CD133, β-catenin and hTERT were detected by immunohistochemical (IHC) method.The relationship of expressions of CD133, β-catenin and hTERT with clinicopathological factors were analyzed.Results Compared with gastritis tissues, the expressions of CD133, β-catenin and hTERT were significantly increased in gastric cancer tissues and precancerous lesions (P<0.01).Compared with the precancerous lesions, the expressions of the above three proteins in gastric cancer were also significantly increased, the difference was also statistically significant (P<0.01).The expressions of CD133, β-catenin and hTERT were not correlated with clinicopathological factors in precancerous lesions, but the expressions of the above three proteins were correlated with lymph node metastasis, differentiation and infiltration depth in gastric cancer (P<0.05).In addition, there were also positive correlations among CD133, β-catenin and hTERT in gastric cancer (P<0.05).Conclusion The co-expressions of CD133, β-catenin and hTERT are closely related to the development of gastric cancer and transformation of precancerous lesions to gastric cancer, which may be key factors for inhibiting the transformation of precancerous lesions to gastric cancer.