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目的:探讨膀胱移行细胞癌Fas/Fasl和c-myc表达与淋巴细胞凋亡及肿瘤免疫逃逸的关系。方法:应用免疫组织化学方法检测50例膀胱癌和15例正常膀胱组织Fas/Fasl和c-myc表达;应用原位末端标记法检测膀胱肿瘤浸润淋巴细胞(TIL)及正常膀胱黏膜浸润淋巴细胞凋亡;分析TIL凋亡率与Fas/Fasl和c-myc的相关性。结果:1)膀胱癌及正常膀胱组织中Fasl光密度值分别为174.54±13.0和143.23±3.88(t=9.287,P<0.01),Fas在膀胱癌组织及正常膀胱黏膜中表达的光密度值分别为126.82±10.09和134.74±4.76,t=3.589,P<0.01。c-myc在膀胱癌组织中表达率为(68.96±16.22)%,在正常膀胱黏膜中不表达。2)TIL凋亡率为(31.47±17.99)%,高于正常膀胱黏膜浸润淋巴细胞的(4.37±1.50)%差异有统计学意义,t=5.795,P<0.01。3)Fasl与TIL凋亡率呈正相关(r=0.85,P<0.01),Fas与TIL凋亡率呈负相关(r=-0.67,P<0.01),c-myc与TIL凋亡率呈正相关,r=0.50,P<0.01。结论:膀胱移行细胞癌Fasl高表达及Fas低表达诱导TIL凋亡,c-myc对该途径起增敏作用,这可能是膀胱肿瘤免疫逃逸的主要机制之一。
Objective: To investigate the relationship between the expression of Fas / Fasl and c-myc in bladder transitional cell carcinoma and lymphocyte apoptosis and tumor immune escape. Methods: The expressions of Fas / Fasl and c-myc in 50 cases of bladder cancer and 15 cases of normal bladder tissues were detected by immunohistochemistry. The infiltration of TIL in bladder tumor and infiltration of lymphocytes in normal bladder mucosa were detected by in situ end-labeling The correlation between TIL apoptosis and Fas / Fasl and c-myc was analyzed. Results: 1) The optical density values of Fasl in bladder cancer and normal bladder were 174.54 ± 13.0 and 143.23 ± 3.88 (t = 9.287, P <0.01), respectively. The optical density of Fas expression in bladder cancer and normal bladder mucosa were 126.82 ± 10.09 and 134.74 ± 4.76, t = 3.589, P <0.01. The expression of c-myc in bladder cancer was (68.96 ± 16.22)%, which was not expressed in normal bladder mucosa. 2) The apoptosis rate of TIL was (31.47 ± 17.99)%, which was significantly higher than that of normal mucosa infiltrating lymphocytes (4.37 ± 1.50)%, t = 5.795, P <0.01.3) (R = 0.85, P <0.01). There was a negative correlation between the apoptosis rate of Fas and TIL (r = -0.67, P <0.01). The positive rate of c- 0.01. CONCLUSION: High expression of Fasl in bladder transitional cell carcinoma and low expression of Fas induce apoptosis of TIL. C-myc can sensitize this pathway, which may be one of the main mechanisms of immune escape in bladder tumor.