摘要
目的探讨促血管生成素-2(Ang-2)、缺氧诱导因子-2α(HIF-2α)及血管内皮生长因子(VEGF)在非小细胞肺癌(NSCLC)组织中的表达及临床意义。方法采用免疫组织化学方法测定59例NSCLC和14例肺部良性病变病理切片中Ang-2、HIF-2α和VEGF的表达并计数微血管密度(MVD),分析其与患者的性别、年龄、病理类型、临床分期、分化程度、肿瘤大小、淋巴结转移情况等临床病理参数的关系。结果 NCCLS组织中,Ang-2、HIF-2α和VEGF的表达率分别为52.5%、71.2%和76.3%,明显高于肺部良性病变组织(P<0.01),且三者两两之间在P=0.01水平上呈明显正相关,Ang-2与VEGF阳性表达组MVD明显高于阴性表达组(P=0.028,P=0.001),且在Ⅲ期NSCLC组织中,Ang-2和VEGF的阳性表达率高于Ⅰ期和Ⅱ期(P<0.05),HIF-2α和VEGF的阳性表达率淋巴结转移阳性组较阴性组高(P<0.05)。结论 Ang-2、HIF-2α和VEGF在NSCLC中均有高表达且与肺癌的新生血管形成有关,并可能影响NSCLC的生物学行为。
Objective To investigate the expression of angiopoietin-2(Ang-2),hypoxia inducible factor-2α(HIF-2α)and vascular endothelial growth factor(VEGF)and the clinical significance in non-small cell lung carcinoma(NSCLC).Methods Immunohistochemistry was used to detect the expression of Ang-2,HIF-2α and VEGF in pathological tissue of 59 cases of NSCLC and 14 cases of non-malignant tissue from lung benign lesions and micro vessel density(MVD)was determined.The relationship between the expression of Ang-2,HIF-2α and VEGF in NSCLC and that with the age,sex,histopathological type,stage,differentiation,size of tumor and lymph node metastasis were analyzed.Results The expression rates of Ang-2,HIF-2α and VEGF in the NSCLC tissue were 52.5%,71.2%and 76.3%,which were significant higher than that in non-malignant tissue,and the expression of Ang-2,HIF-2α,VEGF was related with each others(P<0.05).MVD of Ang-2 and VEGF positive groups was significantly higher than the negative group(P=0.028,P=0.001).In stageⅢ NSCLC,Ang-2 and VEGF expression was higher than in stageⅠandⅡ(P<0.05).The lymph node metastasis rate was higher in HIF-2α and VEGF positive group than in negative group(P<0.05).Conclusions Overexpressions of Ang-2,HIF-2α and VEGF occurred in most cases of NSCLC which may play a critical role of angiogenic factors in the angiogenesis of NSCLC,and potentially be used in assessment of the biologic behavior and prognosis of NSCLC.
出处
《中华临床医师杂志（电子版）》
CAS
2012年第21期6685-6689,共5页
Chinese Journal of Clinicians(Electronic Edition)
基金
国家自然科学基金青年科学基金(81101550)
