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目的探讨非小细胞肺癌(non-small-cell lung cancer,NSCLC)中谷胱甘肽S-转移酶-π(glutathione transferase-πGST-π)、P-糖蛋白(P-glucose protein)与半胱氨酸蛋白酶(Caspase-3)之间的关系以及他们的表达与临床意义。方法采用免疫组织化学法检测117例NSCLC中GST-πPgp的表达水平,流式细胞技术检测Caspase-3的表达;根据肿瘤耐药机制的不同,选择一个凋亡抑制元素与两个耐药元素对肿瘤的耐药进行多方面的分析评估。结果GST-πPgp的阳性率明显高于对照组(P<0.01),PgP与肿瘤的分型无关(P>0.05),两者在分期分化表达中随其差别增大、差异性增加,而产生统计学意义(P<0.05),Pgp在淋巴转移中高表达,GST-π与肿瘤的分型、分期、转移均无关(P>0.05);在分化表达中与前者相同。Caspase-3定量分析中,癌组与对照组、鳞癌与腺癌组、高中低分化组、淋巴转移与无淋巴转移组均有不同程度的统计学意义。结论Pgp高表达时对肿瘤的原发耐药增强,结合Caspase-3定量分析,凋亡指数均有不同程度的衰减。通过生物学行为研究,了解凋亡抑制是肿瘤耐药的主要原因,这有助于临床正确制订初始化疗方案和判断预后。
Objective To investigate the effects of glutathione transferase-πGST-π, P-glucose protein and cysteamine in non-small-cell lung cancer (NSCLC) The relationship between acid protease (Caspase-3) and their expression and clinical significance. Methods The expression of GST-πPgp was detected by immunohistochemistry in 117 cases of NSCLC. The expression of Caspase-3 was detected by flow cytometry. According to the mechanism of tumor resistance, one inhibitor of apoptosis and two drug-resistant elements Cancer drug resistance is evaluated in many ways. Results The positive rate of GST-πPgp was significantly higher than that of the control group (P <0.01). PgP was not associated with the tumor type (P> 0.05), but the difference was significant Pgp was highly expressed in lymphatic metastasis (P <0.05). GST-π was not associated with tumor type, stage and metastasis (P> 0.05), but was similar to the former. Caspase-3 quantitative analysis of cancer and control groups, squamous cell carcinoma and adenocarcinoma group, high school poorly differentiated group, lymph node metastasis and non-lymph node metastasis groups have varying degrees of statistical significance. Conclusion The primary resistance of Pgp to tumor increased when combined with Caspase-3 quantitative analysis, and the apoptotic index decreased to some extent. Through the study of biological behavior, it is known that apoptosis inhibition is the main reason of tumor resistance, which is helpful for the correct formulation of initial chemotherapy regimen and judgment of prognosis in clinic.