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作 者:陈建欧 万丽[2] 陈霖[2] 黄卡特[2] 吴秀玲[2]
机构地区:[1]温州市第八人民医院病理科,浙江温州325000 [2]温州医学院附属第一医院病理科,浙江温州325000
出 处:《温州医学院学报》2012年第4期339-341,345,共4页Journal of Wenzhou Medical College
基 金:温州市科技局科研基金资助项目(Y20090083)
摘 要:目的:探讨FOXP1和pVHL在肾透明细胞癌(CCRCC)中的表达水平及其与临床病理特征的关系。方法:采用免疫组化法检测48例CCRCC中FOXP1和pVHL两种蛋白的表达,并对其与临床分期、病理分级、淋巴结转移等作相关性分析。结果:48例CCRCC中FOXP1阳性表达率为83.3%(40/48),其中3例呈胞膜、胞浆同时表达,9例呈胞核、胞浆同时表达,余28例仅呈胞浆表达。高级别(G3)CCRCC中FOXP1的阳性表达率明显低于低级别(G1、G2)CCRCC(P<0.05)。FOXP1与临床分期、淋巴结有无转移无明显相关性(P>0.05)。pVHL阳性表达率为52.1%(25/48),均为胞浆、胞膜表达。pVHL表达与病理分级、临床分期及淋巴结有无转移均无明显相关性(P>0.05)。9例FOXP1胞核、胞浆同时阳性的CCRCC中8例pVHL阳性,余31例FOXP1胞浆或胞膜表达的CCRCC仅17例pVHL阳性,FOXP1胞核表达与pVHL表达两者具有正相关性关系(r=0.594,P<0.05)。结论:FOXP1胞作为一种潜在的肿瘤抑制基因,在CCRCC中存在高表达,并可能参与肿瘤的发生。FOXP1胞核表达与pVHL表达的相关性提示两者可能存在某种调节机制。Objective: To investigate the expressions of FOXP1 and pVHL in renal clearcell carcinoma (RCC) and their clinical significance. Methods: The expressions of FOXP1 and pVHL in RCC were evaluated immunohistochemically by the two-step detection system (EnVision), and the correlation among their expressions, clinical stage, pathological grade and lymph node metastasis were analyzed. Results: FOXP1 expressed in 83.3% of (40/48) the RCC cases, 3 of 48 cases showed membrane and cytoplasm staining, while 9 cases were stained in nuclear and cytoplasm, 28 cases were stained in cytoplasm, FOXP1 expression in high grade (G3) cases was significantly lower than those in low grade (G1 and G2) (P〈0.05). There was no correla- tion between FOXPI, clinical stage, pathological grade and lymphonode metastasis(P〉0.05). pVHL expressed in 52.1% (25/48) of the RCC cases, all of cases showed membrane and cytoplasm staining, pVHL expression did not significantly correlate with clinical stage, pathological grade and lymphonode metastasis(P〉0.05). Eight of 9 cases with FOXPI nuclear and cytoplasm staining pattern showed pVHL positive simultaneously, There was statistically positive correlation between FOXP1 and pVHL expression. (r=0.594, P〈0.05). Conclusion: As a poten- tial tumor suppressor gene, FOXP1 is highly expressed in RCCs and may participate tumorogensis, It may presence a mechanism between FOXP1 protein and pVHL protein.
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