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目的 观察逆转录病毒介导的单纯疱疹病毒胸苷激酶 (HSV TK)、共刺激因子 (B7)基因联合治疗乳腺癌的作用 ,并探讨其作用机理。方法 应用基因重组技术 ,构建携带TK/B7基因的逆转录病毒载体。在 80只SD大鼠乳腺癌模型上 ,分别于瘤体内注射基因转染的乳腺癌细胞 ,3d后腹腔内连续 15d注射更昔洛韦 (GCV) 5 0mg·kg-1·d-1。用 4h51Cr释放法检测脾细胞毒T淋巴细胞(CTL)活性。结果 TK组瘤细胞大量凋亡 ;B7组淋巴细胞聚集 ;TK +B7组肿瘤细胞凋亡 ,并可见淋巴细胞的聚集。CTL活性分别为 :对照组 (35 .6± 2 .7) %、TK组 (39.2± 3.8) %、B7组 (6 7.4±4.3) %、TK +B7组 (6 2 .1± 3.5 ) % ,B7、TK +B7组较对照组、TK组显著增强 (P <0 .0 1)。结论 HSV TK、B7联合基因治疗大鼠乳腺癌 ,具有直接杀伤肿瘤和增强机体抗肿瘤免疫双重作用。
Objective To observe the effect of retrovirus-mediated herpes simplex virus thymidine kinase (HSV TK) and co-stimulatory factor (B7) gene therapy on breast cancer, and to explore its mechanism of action. Methods Gene recombination technology was used to construct a retroviral vector carrying TK/B7 gene. In 80 SD rat mammary carcinoma models, gene-transfected breast cancer cells were injected intratumorally. After 3 days, ganciclovir (GCV) 50 mg·kg-1·d-1 was continuously injected intraperitoneally for 15 days. Splenocyte cytotoxic T lymphocyte (CTL) activity was measured by 4h51Cr release assay. Results The tumor cells in the TK group had a large number of apoptosis; lymphocytes in the B7 group were aggregated; tumor cells in the TK+B7 group were apoptotic and lymphocyte aggregation was observed. The CTL activity was: 35.6±2.7% in the control group, 39.2±3.8% in the TK group, 67.4±4.3% in the B7 group, and 62.1±3.5% in the TK+B7 group. , B7, TK +B7 group than the control group, TK group significantly enhanced (P <0. 01). Conclusion HSV TK and B7 combined gene therapy for breast cancer in rats has direct effects on killing tumors and enhancing anti-tumor immunity.