肾癌中EphA2和EphrinA1的表达及其与微血管密度的关系

目的 探讨EphA2和EphrinA1在肾癌组织中的表达,及其与肿瘤血管生成的关系.方法 应用用免疫组化法检测68例肾癌组织、24例正常肾组织中EphA2和EphfinA1的表达,采用CD34抗体标记微血管内皮细胞,计算微血管密度(MVD).结果 肾癌组织中EphA2和EphrinA1蛋白的表达明显高于正常肾组织(均P<0.01).正常肾组织中MVD为25.23±7.09,肾癌组织中MVD为39.68±7.24,差异有统计学意义(P<0.01).在肾癌组织中,分化程度为2、3级组的EphA2和EphrinA1蛋白表达水平高于分级为1级组(P<0.01,P<0.05),分期为Ⅲ、Ⅳ期组高于Ⅰ、Ⅱ期组(P<0.01,P<0.05),有淋巴结转移组高于无淋巴结转移组(P<0.05);肿瘤直径≥7 cm组的MVD高于<7 cm组(P<0.05),分化程度为2、3级组高于1级组(P<0.01),分期为Ⅲ、Ⅳ期组高于Ⅰ、Ⅱ期组(P<0.05),有淋巴结转移组高于无淋巴结转移组(P<0.01).相关分析结果显示,EphA2、EphrinA1的表达与MVD呈正相关(r分别为0.555和0.485,均P<0.01).结论 EphA2和EphrinA1在肾癌组织中高表达,并与肿瘤的分化程度、临床分期、肿瘤血管生成有关.

Expression of EphA2 and EphrinA1 in human renal cell carcinoma and its relationship with angiogenesis

Objective To investigate the expression of EphA2 and EphrinA1 and its relationship with angiogenesis in renal cell carcinoma and its relevance to clinicopathologic features. Methods The expression of the EphA2 and EphrinA1 was detected by immunohistochemistry (IHC) in the tissues samples from 68 renal cell carcinomas and 24 normal kidneys, and quantitatively analyzed. The microvessel density (MVD) was determined by CD34 immunestaining of microvascular endothelial cells. Statistical analysis was performed using the software SPSS ( version 13.0). Results The expression of EphA2, EphrinA1 and MND in the cancerous tissues were significantly higher ( P < 0. 01 ) than that in the normal ones. Significantly increased expression of EphA2, EphrinA1 and MVD ( P <0.01 ) was detected in cancer tissues with higher grade differentiation, more advanced stage and more lymph node metastasis, respectively (P < 0.05 for each group). Expression of the EphA2 and EphrinA1 protein was shown to be positively associated with the MVD assessed by Spearman's correlation and factor analysis (r = 0. 555, r = 0. 485, P < 0. 01 ). The MVD was also significantly correlated with the diameter of the tumor ( P < 0. 01 ). Conclusion EphA2 and EphrinA1 are highly expressed in renal cell carcinoma, and positively correlated with histological differentiation, clinical stage and angiogenesis in the cancer.