血管生成素-1和血管生成素-2在喉鳞状细胞癌中的表达及与血管生成的关系

目的:研究喉鳞状细胞癌(LSCC)中血管生成素-1,2(Ang-1,2)的表达及与临床病理学特征、CD105标记的微血管密度(MVD)之间的关系,评估Ang-1,2及血管内皮生长因子(VEGF)在LSCC中的联合表达对肿瘤血管生成的作用。方法:用常规免疫组织化学法检测LSCC标本61例、癌旁组织30例及正常喉黏膜组织15例中Ang-1,2及VEGF的表达和MVD,并对临床病理资料进行回顾性分析。结果:Ang-1,2在LSCC细胞、正常喉黏膜上皮细胞及血管内皮细胞均有表达;VEGF只表达于LSCC组织中;LSCC组织与癌旁组织及正常喉黏膜组织相比,Ang-1,2表达显著增加(均P<0.05)。对于临床病理因素的分析表明,Ang-1,2在高、中低分化LSCC中的表达差异无统计学意义(均P<0.05);Ang-2表达与临床分期、MVD有显著的相关性(均P<0.05),而Ang-1的表达与临床分期、MVD无显著的相关性(均P>0.05)。在所有联合表达状态中Ang-2和VEGF同时为阳性的肿瘤组织MVD均值为最高,显著高于其他任何状态(P<0.05)。结论:Ang-1,2在LSCC中的表达可能在肿瘤进展过程中起了重要的作用,与肿瘤血管的形成关系密切。其中Ang-2与VEGF共同作用促进肿瘤血管的形成。

Expression of angiopoietin-1,2 and its relationship with angiogenesis in laryngeal squamous cell carcinoma

Objective:To investigate the expression of Angiopoietin-1,2 in laryngeal squamous cell carcinoma(LSCC) and the relationship between Angiopoietin-1,2 expression and clinicopathologic parameters and microvessl density(MVD) marked by CD105,and also evaluate the significance of co-expression of Ang-2 and vascular endothelial cell growth factor(VEGF) in tumor angiogenesis.Method:The expression of Ang-1,2 and VEGF in samples of tumor,para cancer and normal mucosa were dectected by immunohistochemical method.Result:The expression of Angiopoietin-1,2 were identified in LSCC,para cancer tissue and normal mucosa.The VEGF expression was only existed in LSCC.The expression of Ang-1,2 were significantly higher in LSCC than in para cancer tissue(P<0.05) and normal mucosa(P<0.01).In the clinicopathologic parameters,only the expression of Ang-2 was closely correlated with clinical stages and MVD(all P<0.05).There was no significant correlation between the expression of Ang-1,2 and tumor differentiation degree(all P>0.05).When the expression of Ang-2 and VEGF were both positive,the mean value of MVD was higher than others(P<0.05).Conclusion:These results suggest that overexpression of Ang-1,2 may play a very important role in the development of LSCC and are closely correlated with angiogenesis.Ang-2 promote angiogenesis when interacting with VEGF.