摘要
目的:探讨大肠癌组织中VEGF-C、Flt-4和Survivin表达与淋巴管生成及淋巴结转移的关系。方法:采用酶组织化学方法及免疫组化方法对32例结肠癌组织中VEGF-C、Flt-4和Survivin的表达及淋巴管的生成进行研究。结果:VEGF-C和Flt-4表达密切相关(P<0.01);VEGF-C阳性淋巴管数较其阴性淋巴管数明显增多(27.16±6.56,19.12±6.34),P<0.01;Flt-4阳性淋巴管数较Flt-4阴性淋巴管数明显增多(27.46±7.32,20.13±7.64),两者表达均与淋巴结转移相关,P<0.05;Survivin阳性淋巴管计数与其阴性淋巴管计数(22.16±6.32,21.97±6.53)差异无统计学意义,P>0.05,三者的表达均与肿瘤的淋巴结转移相关。结论:Survivin影响VEGF-C的活性,VEGF-C可以激活间质中的Flt-4从而刺激淋巴管增生,为肿瘤细胞的淋巴结转移提供了必要的条件。
OBJECTIVE: To investigate the expressions of VEGF-C, Flt-4, Survivin and thire relationship with lymphangiogenesis and metastasis of lymph node in coloreetal carcinoma tussues. METHOD: The expressions of VEGF-C, Flt-4 and Survivin were determined by immunohistochemistry (SP) and lymphatic vessles were stained by the enzyme histochemical method in 32 cases of coloreetal carcinomas. RESULTS: There was a significant correlation between the expressions of VEGF-C and Flt-4 in coloreetal carcinoma (P〈0. 01). The number of lymphatic vessels in VEGF-C positive tumor was significantly larger than that in VEGF-C negative tumor (27. 16 ±6.56, 19. 12±6. 34, P〈0. 01). Similarly, the number of lymphatic vessels in Flt-4 positive tumors was larger than that in Flt-4 negative tumor (27. 46 ±7. 32, 20. 13±7. 64) (P〈0. 05). Both the exprecsions of VEGF-C and Flt-4 were closely belated to the lymph node metastasis. There was no significant difference between the number of lymphatic vessels in Survivin positive and negative tumors ( 22. 16 ± 6.32, 21. 97 ± 6. 53 ), P 〉 0. 05. The expressions of VEGF-C, Flt-4 and Survivin were related to the metastasis of lynph nodes. CONCLUSION: Survivin affects the activities of VEGF-C. VEGF-C may activate flt-4 in matrix and stimulate the proliferations of lymphatic vessels, which might provide necessary conditions for the metastasis of lymph nodes in coloreetal carcinoma.
出处
《中华肿瘤防治杂志》
CAS
2007年第16期1232-1234,共3页
Chinese Journal of Cancer Prevention and Treatment
关键词
结肠肿瘤/病理学
受体
血管内皮生长因子/代谢
淋巴转移
免疫组织化学
colonic neoplasms/pathology
receptors, vascular endothelial growth factor/metabolism
lymphaticmetastasis
immunhistochemistry