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目的:检测HBV感染型及非HBV感染型肝细胞肝癌组织中VEGF及CD34表达情况,探讨与肿瘤血管生成的关系。方法:共收集四川省人民医院手术切除经病理证实的肝细胞肝癌标本61例,根据血清学及免疫组化法检查HBs Ag,采用随机数字表法进行分组,将其分为HBV感染组和非HBV感染组。免疫组化SABC法检测两组中VEGF及CD34的表达情况,并行微血管密度值(MVD)计数。比较肝癌组织中不同VEGF表达组间MVD值计数,分析肝癌组织中VEGF的表达及MVD计数与肝癌临床病理特征的关系。结果:HBV感染组VEGF及CD34阳性表达率分别为72.22%及55.56%,显著高于非HBV感染组(阳性表达率分别为40.00%及28.00%,P<0.05),且HBV感染组的MVD值明显高于非HBV感染组(P<0.05)。VEGF阳性组的MVD值明显高于VEGF阴性组(P<0.05)。不同性别、年龄、肿瘤直径及有无门静脉癌栓肝癌患者的肝癌组织MVD值、VEGF的表达比较差异均无统计学意义(P>0.05),而不同TNM分期,不同肝癌组织Edmondson病理分级患者的MVD值、VEGF表达比较,差异有统计学意义(P<0.05),随着TNM分期及病理分级的增加,肝癌组织的MVD计数及VEGF表达均显著增加;同时,HBe Ag阴性患者的MVD计数及VEGF表达显著高于HBe Ag阳性患者(P<0.05)。结论:HBV感染型肝癌组织中VEGF、CD34的表达及MVD值显著高于非HBV感染组,HBV感染可能上调肝癌组织中VEGF及CD34的表达。过度表达的VEGF及CD34促进了肿瘤的血管生成有助于肿瘤的进一步浸润和转移。
Objective: To detect the expression of VEGF and CD34 in hepatocellular carcinoma of HBV-infected and non-HBV-infected hepatocellular carcinoma (HCC), and to explore the relationship with VEGF and tumor angiogenesis. Methods: Totally 61 cases of pathologically confirmed hepatocellular carcinoma (HCC) were collected from Sichuan Provincial People’s Hospital. HBsAg was detected by serological and immunohistochemical methods and divided into HBV infection group and non-HBV group HBV infection group. Immunohistochemical SABC method was used to detect the expression of VEGF and CD34 in both groups, and the microvessel density (MVD) was counted. To compare the MVD value between different VEGF expression groups in hepatocellular carcinoma and to analyze the relationship between the expression of VEGF and the clinicopathological features of hepatocellular carcinoma in patients with hepatocellular carcinoma. Results: The positive rates of VEGF and CD34 in HBV infection group were 72.22% and 55.56%, respectively, which were significantly higher than those in non-HBV infection group (the positive rates were 40.00% and 28.00% respectively, P <0.05) Significantly higher than non-HBV infection group (P <0.05). The MVD of VEGF-positive group was significantly higher than that of VEGF-negative group (P <0.05). There were no significant differences in MVD and VEGF expression between HCC patients with different gender, age, tumor diameter and with or without portal vein tumor thrombus (P> 0.05). However, there was no significant difference between MVD and VEGF expression in patients with Edmondson pathology MVD and VEGF expression were significantly different (P <0.05). With the increase of TNM stage and pathological grade, MVD and VEGF expression in HCC were significantly increased. Meanwhile, the MVD counts in patients with HBeAg-negative and VEGF expression was significantly higher than HBeAg-positive patients (P <0.05). Conclusion: The expression of VEGF, CD34 and MVD in HBV-infected HCC tissues were significantly higher than those in non-HBV-infected HCC tissues. HBV infection may up-regulate the expression of VEGF and CD34 in HCC tissues. Overexpression of VEGF and CD34 promote tumor angiogenesis contribute to further tumor invasion and metastasis.