喉鳞状细胞癌血管生成和凋亡的表达及其相关性研究

目的:探讨血管生成与喉鳞状细胞癌自发性细胞凋亡及临床病理特征的关系。方法:采用免疫组织化学SABC方法及原位组织尿嘧啶脱氧核糖核苷酸末断转移酶介导的缺口末断标记(TUNEL)技术检测34例喉鳞状细胞癌中瘤内微血管密度(IMVD)、细胞凋亡指数(AI)及血管内皮生长因子(VEGF)的表达。结果:34例喉鳞状细胞癌中平均IMVD为21.50±8.87,AI中位数为1.15%。有、无颈淋巴结转移组平均IMVD分别为26.33±9.70、17.68±6.06,其差异有统计学意义(P<0.01);组织学分级高、中、低分化组平均IMVD差异有统计学意义(P<0.01),两两比较,高、中分化组差异有统计学意义(P<0.05);VEGF表达与IMVD呈显著正相关(r=0.51,P<0.01);IMVD与AI呈显著负相关(r=-0.53,P<0.01);IMVD与喉癌T分期无关。结论:IM-VD可作为预测喉癌颈淋巴结转移的重要指标;VEGF是一个重要的血管生成因子,可促进喉癌血管生成;血管生成可抑制喉癌自发性细胞凋亡,从而促进喉癌的恶性进展。

Study on the expression of angiogenesis and spontaneous apoptosis and their relevance in laryngeal squamous cell carcinoma

OBJECTIVE: To investigate the relationship among angiogenesis, spontaneous apoptosis and clinicopathological parameters in laryngeal squamous cell carcinoma (LSCC). METHOD: The intratumor microvessel density (IMVD), apoptotic index (AI) and vascular endothelial growth factor (VEGF) expression were detected by immunohistochemistry SABC and terminal uridine deoxynucleotidyl transferase mediated nick end labeling(TUNEL) methods in34 LSCC patients. RESULT: The average IMVD was (21.50 +/- 8.87), and median of AI was 1.15%. The average IMVD in positive and negative cervical lymphatic metastasis was (26.33 +/- 9.70) and (17.68 +/- 6.06) respectively, and the IMVD with positive lymphatic metastasis tumors was statistical significantly higher than those with negative cervical lymphatic metastasis tumors (P < 0.01). The average IMVD had statistical difference in histological grading (P < 0.01), and analysis by one to one, the average IMVD had statistical difference between high and median grading. Expression of VEGF had a significantly positive correlation with IMVD (r = 0.51, P < 0.01). Statistical analysis revealed a significantly inverse correlation between AI and IMVD (r = -0.53, P < 0.01). We failed to find the statistical difference between IMVD and tumor T-stage in LSCC. CONCLUSION: IMVD may be an important indicator to predict cervical lymphatic metastasis in LSCC. VEGF might be an important angiogenic factor, and could promote tumor angiogenesis in LSCC. Tumor angiogenesis might contribute to tumor malignant progression by inhibiting spontaneous apoptosis in LSCC.