uPASNVEGF在脑膜瘤、胶质瘤、脑转移癌中的表达及意义

背景与目的：肿瘤的生长须依赖新生血管的生成，而目前认为血管内皮生长因子(vascular endothelial growth factar，VEGF)、尿激酶型纤溶酶原激活物(urokinase—type plasminogen activator，uPA)是刺激肿瘤血管形成和肿瘤浸润过程中的重要因子．本文探讨VEGF和uPA在脑膜瘤、胶质瘤、脑转移癌中的表达及临床意义。方法：应用免疫组化法检测30例脑膜瘤、30例脑转移癌、40例胶质瘤及10例正常脑组织中uPA和VEGF的表达，并结合临床资料分析。结果：vEGF与uPA在三种肿瘤中均有表达；VEGF和uPA表达与瘤周水肿程度呈正相关；VEGF和uPA表达与胶质瘤恶性程度呈正相关。结论：检测vEGF和uPA对脑膜瘤、胶质瘤、脑转移癌的生物学行为、瘤周水肿和预后评估有参考价值。     

Neogenin表达下调与神经胶质瘤发生、发展的关系

背景与目的：神经胶质瘤是中枢神经系统最常见肿瘤,其发病机制尚不明确。Neogenin表达异常与多种癌症进展及预后相关．是一个潜在的肿瘤抑制因子。本研究的目的在于阐明Neogenin在神经胶质瘤发生和进展过程中的作用。方法：通过对小鼠正常脑组织及人神经胶质瘤组织及肿瘤周边脑组织进行免疫组织化学方法染色．分析Neogenin在正常脑组织及肿瘤组织中的细胞内分布差异,以及其在胶质瘤中表达水平较其周边脑组织表达的差别：进一步分析其在不同级别胶质瘤中的表达水平差异;最后通过MSP法分析Neogenin在神经胶质瘤中的启动子甲基化水平。结果：我们发现Neogenin在小鼠脑中表达丰富,主要位于神经胶质细胞的胞膜上;Neogenin在肿瘤区域的平均表达水平较周边区域低,其在肿瘤区域主要胞浆内呈弥散分布。对69例原发胶质瘤患者的肿瘤组织进行免疫组织化学分析．进一步确认了Neogenin在神经胶质瘤中表达水平与肿瘤的恶性程度呈负相关（One-Wav ANOVA,n=69,P〈0．01）。通过甲基化特异性PCR法分析表明,Neogenin的启动子在37．5％（3／8）的人神经胶质瘤组织中存在甲基化．但是我们存3株人脑胶质瘤细胞系中未检测到Neogenin启动子甲基化现象。结论：Neogenin与神经胶质瘤的发生、发展有关,其启动子部分甲基化可能是导致Neogenin表达下渊的原因之一．这种表达下调为神经胶质瘤的起源、发展提供了选择性优势。     

胶质瘤患者血清VEGF、bFGF及uPA定量分析的临床价值

目的：探讨胶质瘤患者血清VEGF，bFGF及uPA水平与胶质瘤及其分级的关系。方法：采用酶联免疫吸附法（ELISA）定量分析40例胶质瘤患者及8例健康人血清VEGF，bFGF及uPA水平，并进行比较分析。结果：Ⅲ，Ⅳ级胶质瘤患者血清VEGF，bFGF水平显著高于I，Ⅱ级者和正常对照组；而胶质瘤患者血清uPA水平显著高于正常对照组，不同级别的胶质瘤其upA水平比较无显著性差异。结论：级别高的胶质瘤患者血清中VEGF，bFGF及uPA水平均有显著性升高，三者可作为临床诊断胶质瘤的辅助指标。     

胃肠道间质瘤（GIST）中TGF-β1与uPA的表达和相关性研究

目的：探讨TGF-β1及uPA在胃肠道间质瘤中的表达以及与胃肠道间质瘤临床病理特征之间的关系,并探讨其临床意义。方法：以124例胃肠道间质瘤患者为研究对象,采用RT-PCR方法检测TGF-β1、uPA在胃肠道间质瘤及对照组的mRNA水平。结果：在胃肠道间质瘤中,TGF-β1与uPA高表达,其表达与性别、年龄、组织类型不相关,而与肿瘤黏膜受侵、NIH分级、肿瘤侵袭转移相关（P〈0.05）。TGF-β1与uPA的表达呈正相关（r=0.420,P〈0.001）。结论：在胃肠道间质瘤中TGF-β1可以上调uPA表达。随着黏膜受侵及侵袭转移的改变和NIH分级的进展,胃肠道间质瘤的肿瘤组织中TGF-β1与uPA的表达逐渐升高。提示TGF-β1、uPA参与了肿瘤的浸润和转移。     

舌鳞癌中uPA及nm23-H1蛋白表达及临床意义

目的：探讨uPA及nm23-H1在舌鳞癌中的表达及与侵袭、转移的关系。方法：采用免疫组织化学方法在蛋白水平检测uPA及nm23-H1在74倒舌癌中的表达。结果：uPA及nm23-H1与舌癌的病理学分级无关。uPA表达与肿瘤颈淋巴结转移呈正相关。nm23-H1表达与肿瘤颈淋巴结转移呈负相关。uPA及nm23-H1的表达率呈负相关。uPA阳性并且nm23-H1阴性表达者．颈淋巴结转移率明显高于uPA阴性并且nm23-H1阳性表达者。结论：UPA及nm23-H1的表达可以作为舌癌淋巴结转移的重要标志：UPA及nm23-H1的表达在舌癌的侵袭特移中可能是一对相互拮抗的因素．联合检测具有一定的临床意义。     

彩色多普勒超声导航在深部神经胶质瘤显微手术中的应用价值

目的：探讨彩色多普勒超声导航技术在深部神经胶质瘤显微手术中的应用价值。方法选择确诊为深部神经胶质瘤且具有手术指征的30例,且这30例患者均应用了彩色超声多普勒导航技术,术前对患者进行了MRI和CT检查定位,进行开颅,暴露出硬脑膜后实时彩色多普勒超声确定深部神经胶质瘤的病变部位、范围、大小及周围血供情况,选择最佳的手术入路,彩色多普勒超声引导下放置明胶引导显微神经外科手术路径,并实时监控、评估病灶切除情况,术后行头颅MRI和CT检查,与术前的检查结果进行对比以评估疗效,同时选取同一时期未采用彩色多普勒超声导航的30例患者作为对照组,比较两组的手术时间及手术全切率。结果低级别与高级别胶质瘤的超声显像具有不同的特征,采用术中超声导航的30例患者的病变均能够准确定位,术中使用彩色多普勒超声导航,可以明显缩短深部神经胶质瘤的手术时间及提高全切率。结论彩色多普勒超声导航可以显著缩短深部神经胶质瘤显微手术的手术操作时间,并且可以做到实时监控,提高了肿瘤的全切率。     

脑胶质瘤O6-甲基鸟嘌呤-DNA甲基转移酶启动区甲基化及其表达异质性的研究

目的研究脑胶质瘤组织不同部位O6-甲基鸟嘌呤-DNA甲基转移酶（MGMT）启动区甲基化状态及其表达的差异性。方法在54例脑胶质瘤组织的中心和周边部位分别获取标本,共获得92份标本,采用巢式甲基化特异性PCR（MSP）进行MGMT启动区甲基化状态的检测,同时采用免疫组织化学方法进行MGMT蛋白表达的检测。结果 38例胶质瘤中获得了肿瘤两个不同部位MG-MT启动区甲基化的状态,其中24例胶质瘤MGMT启动区甲基化的状态是一致的,占总数的63.2%（24/38）。在29例胶质瘤患者中获得了肿瘤两个不同部位MGMT蛋白表达的情况,其中10例胶质瘤MGMT蛋白表达是一致的,占总数的34.5%（10/29）。两总体一致性概率间差值的95%置信区间为（5.6%和51.8%）,两者的差异有统计学意义。巢式MSP和免疫组化都获得检测结果的标本有77份,在61份MGMT启动区甲基化标本中,25份MGMT蛋白表达阴性,14份蛋白表达可疑阳性,18份蛋白表达阳性,4份蛋白表达强阳性。在16份MGMT启动区非甲基化标本中,2份MGMT蛋白表达阴性,2份蛋白表达可疑阳性,9份蛋白表达阳性,3份蛋白表达强阳性,MGMT启动区甲基化状态与蛋白表达呈负相关（r=-0.318,P=0.005）。结论脑胶质瘤MGMT蛋白表达在同一肿瘤的不同部位存在明显的异质性。虽然脑胶质瘤MGMT启动区甲基化的状态在同一肿瘤的不同部位存在一定的异质性,但是大多数脑胶质瘤MGMT启动区甲基化的状态在同一肿瘤的不同部位是一致的。脑胶质瘤MGMT启动区甲基化状态的一致性优于蛋白表达的一致性。脑胶质瘤MGMT启动区甲基化,MGMT蛋白表达较少,MGMT启动区非甲基化,MGMT蛋白表达较多。     

基质金属蛋白酶对胶质瘤干细胞侵袭作用的影响

目的:分别在体内及体外条件下,观察恶性胶质瘤肿瘤干细胞(CancerStemCells,CSCs)的侵袭能力,检测恶性胶质瘤不同细胞亚群的基质金属蛋白酶-2(MMP-2)和-9(MMP-9)的表达,探讨其与CSCs侵袭能力的相关性.方法:应用神经干细胞(neural stem cells,NSCs)培养基体外分离培养原代恶性胶质瘤细胞,应用自我更新分析、免疫细胞化学染色、体内成瘤分析等技术鉴定CSCs细胞亚群.分别在体内、体外条件下,应用细胞侵袭分析技术观察不同肿瘤细胞亚群的侵袭能力,应用实时RT-PCR、Western blot、免疫组织化学染色方法,检测不同肿瘤细胞亚群中MMP-2、MMP-9的表达情况.结果:原代培养的恶性胶质瘤细胞被分离鉴定为CSCs和非肿瘤干细胞(non-CSCs).胶质瘤CSCs的促侵袭能力明显强于non-CSCs;MMP一2的表达水平在两个细胞亚群间存在显著差异(P<0.000 1).且均明显高于MMP-9表达;在胶质瘤CSCs接种的动物脑组织中,MMP-2与MMP-9的表达均呈时间依赖性增高,MMP-9则仅在肿瘤组织中表达,其表达增长率高于MMP-2,且主要定位于肿瘤的边缘.结论:在不同的条件下,胶质瘤CSCs可能是通过MMP-2或MMP-9促进了肿瘤细胞的侵袭及肿瘤的侵袭性生长.特异性抑制胶质瘤CSCs明胶酶分泌,尤其是MMP-9,将为抗肿瘤治疗提供有效的手段.未来针对于CSCs与其它MMPs家族成员及其抑制剂的研究将有利于进一步阐述胶质瘤的侵袭机制,同时也将为抗恶性胶质瘤的治疗提供新的策略.     

干细胞标志物CD133和Nestin在不同恶性程度胶质瘤组织中的表达及其与预后的关系

背景与目的：近来研究表明,胶质瘤中一小群表达干细胞标志的细胞是胶质瘤发生及发展的根源。本文探讨干细胞标志物CD133和Nestin在不同恶性程度人脑胶质瘤组织中的表达情况及其与预后的关系。方法：应用实时荧光定量PCR方法定量检测77例不同恶性程度胶质瘤组织中CD133和Nestin基因的表达情况,并与肿瘤的恶性程度进行相关分析;探讨肿瘤组织中上述基因的表达水平与患者预后的关系。结果：在不同恶性程度胶质瘤组织中,CD133及Nestin的表达存在显著性差异（P〈0.05）,CD133和Nestin的表达情况与肿瘤的恶性程度呈正性相关（P〈0.05）;单因素预后分析显示CD133和Nestin的表达水平与预后相关（P〈0.05）,CD133和Nestin基因的高表达预示一个较短的生存时间;多因素Cox比例风险回归模型分析显示,CD133是独立于病理级别及其他临床变量的预后因子。结论：检测胶质瘤组织中CD133和Nestin的表达水平有助于评价肿瘤的生物学行为和患者的预后。     

尿激酶纤溶酶原激活物和基质金属蛋白酶-9在结直肠癌中表达及意义

[目的]研究尿激酶纤溶酶原激活物(uPA)、基质金属蛋白酶-9(MMP-9)在大肠癌中的表达及其意义。[方法]应用免疫组化SP法检测大肠癌术后标本中uPA、MMP-9蛋白的表达情况,并分析不同病理特征间的uPA、MMP-9蛋白的表达情况。[结果]在75例大肠癌中,uPA阳性表达率为28.0%(21/75)。uPA阳性表达率与肿瘤大小相关,肿瘤>4cm者uPA阳性率为42.3%(11/26);而肿瘤≤4cm者uPA阳性率为20.4%(10/49)(χ2=4.041,P=0.044)。MMP-9阳性表达率为33.3%(25/75)。肿瘤>4cm者MMP-9阳性率为50.0%(13/26);而肿瘤≤4cm者MMP-9阳性率为24.5%(12/49)(χ2=4.974,P=0.026)。[结论]uPA和MMP-9共同促进了肿瘤的发生发展及侵袭和转移。联合检测MMP-9、uPA的表达情况对于评估大肠癌的发展及预后具有重要意义。     

RANKL、RANK蛋白在胶质母细胞瘤组织中的表达及临床意义

目的:分析RANKL、RANK蛋白在胶质母细胞瘤组织中的表达及临床意义。方法:收集2017年10月至2019年10月于我科行手术治疗的21例胶质母细胞瘤患者的临床资料，用蛋白印迹试验检测肿瘤中心组织、瘤周组织、皮层造瘘脑组织中RANKL、RANK表达情况，并对其进行统计学分析。结果:肿瘤中心组织RANKL表达高于瘤周组织，有统计学差异(P=0.032)；瘤周组织高于皮层造瘘脑组织，有统计学差异(P=0.024)。瘤周组织RANK表达明显高于肿瘤中心组织，有统计学差异(P=0.006)；肿瘤中心组织高于皮层造瘘脑组织，有统计学差异(P=0.028)。结论:肿瘤中心组织中RANKL表达高于瘤周组织、脑组织，而瘤周组织中RANK明显高于肿瘤中心组织、肿瘤中心组织高于脑组织，我们认为RANKL/RANK通路可能在胶质母细胞瘤侵袭过程中起重要作用，有待后续进一步试验。     

尿激酶型纤溶酶原激活因子基因与胶质瘤的侵袭及预后的关系

目的探讨尿激酶型纤溶酶原激活因子（ｕＰＡ）基因表达与胶质瘤发展及预后的关系。方法采用Ｎｏｒｔｈｅｒｎ印迹分子杂交和免疫组化方法检测４３例人脑胶质瘤和５例正常脑组织,其ｕＰＡｍＲＮＡ和蛋白表达,并结合临床生物学参数进行综合分析。结果上述组织或细胞均可表达２．５ｋｂ的ｕＰＡｍＲＮＡ转录物,高级别胶质瘤较低级别和正常脑组织ｕＰＡｍＲＮＡ表达水平明显增高（Ｐ＜０．０１）;低级别胶质瘤与正常脑组织的表达无显著差异（Ｐ＞０．０５）;术后１８个月内复发和生存期小于３年者,ｕＰＡｍＲＮＡ表达显著高于术后１８个月无复发及生存期大于３年者（Ｐ＜０．０１）;ｕＰＡｍＲＮＡ表达水平与胶质瘤微血管数量呈显著相关（ｒ＝０．５６,Ｐ＜０．０１）,与患者性别、年龄及肿瘤大小无显著相关（Ｐ＞０．０５）。ｕＰＡ蛋白主要分布在胶质母细胞瘤、间变性星形细胞瘤组织的瘤细胞及内皮细胞,低级别胶质瘤较少。结论ｕＰＡ基因表达与人脑胶质瘤恶性度、侵袭性及血管生成有关,对胶质瘤的复发和预后有一定意义。     

CD34、p53在脑多形性黄色星形细胞瘤及巨细胞胶质母细胞瘤中的表达及意义

目的：探讨CD34、p53在多形性黄色星形细胞瘤（PXA）及巨细胞胶质母细胞瘤（GCG）中的表达情况,以及两种肿瘤的临床病理特点、诊断及鉴别诊断。方法：对13例PXA及11例GCG进行临床病理学观察,CD34、p53等免疫组化分析。结果：PXA患者组织学特征： 肿瘤由巨怪瘤细胞、梭形细胞和泡沫样瘤细胞组成,有丰富的网状纤维及淋巴细胞浸润,坏死和核分裂象少见。GCG患者组织学特征： 瘤细胞多形性,以巨怪形瘤巨细胞为主,核分裂象和出血坏死多见,网状纤维沿血管周围分布,有淋巴细胞浸润。CD34在11例PXA中呈弥漫阳性表达,而在GCG中无一例阳性表达;p53在11例GCG中的阳性表达率达到60%-90%以上,而在PXA中的阳性率小于5%。结论：PXA及GCG临床、病理组织形态相似而预后完全不同,两者鉴别诊断的要点在于瘤细胞的异型性、核分裂象、坏死等。CD34、p53的免疫组化染色在两种肿瘤鉴别诊断中有重要意义。     

Evaluation of urinary plasminogen activator, its receptor, matrix metalloproteinase-9, and von Willebrand factor in pancreatic cancer.

PURPOSE: Pancreatic cancer remains a devastating problem with the majority of patients succumbing to death from this disease. A hallmark of pancreatic cancer is the loss of basement membrane that may be attributed to the action of urinary plasminogen activator (uPA) and matrix metalloproteinase-9 (MMP-9). These enzymes are also implicated in angiogenesis. uPA and microvessel density have been shown to be good prognostic indicators for breast and colon cancer. MMP-9 and microvessel density have not been investigated in pancreatic cancer. We have therefore investigated by immunohistochemistry: (a) frequency of uPA expression and its receptor uPAR and the site of synthesis of uPA by in situ hybridization (ISH); (b) MMP-9 and its coexpression with uPA; (c) microvessel density as determined by von Willebrand factor staining and its relationship to uPA and MMP-9 expression; and (d) correlation of these parameters with survival. EXPERIMENTAL DESIGN: Archival paraffin sections of 27 pancreatic tumors were semiquantitatively investigated by immunohistochemistry using the following antibodies: (a) monoclonal antibodies (MAbs) uPA(1) and uPA(2) (3689 and 394, respectively); (b) MAb uPAR, (no. 3932); (c) MAb MMP-9 (no. 936); and (d) rabbit anti-F8RA/vWF. ISH was performed using a uPA cDNA. RESULTS: Both uPA antibodies revealed overexpression of uPA (93%) often with uniform staining of tumor cells. uPAR and MMP-9 showed focal staining in only 52 and 37% of tumors, respectively. Morphologically normal appearing ductal cells in close proximity to tumors overexpressed uPA in contrast to distally located normal cells (P = <0.001). uPA staining was also investigated in pancreatic intraepithelial neoplasia (PanIN) lesions. PanIN 1A/B staining for uPA was seen in 8 cases (30%), that for PanIN 2 in 19 cases (70%), and for PanIN3 in 12 cases (44%). Lumen of microvessels in the tumor stroma also revealed staining of uPA in 10 cases (37%). ISH experiments revealed the presence of uPA mRNA not only in the cytoplasm of tumor cells but also in adjacent normal appearing ducts as well as in PanIN lesions. Patients with overexpression of uPA, uPAR, or MMP-9 had a trend toward poorer survival than those who did not express it. Microvessel density did not show any significant relationship with uPA, uPAR, and MMP-9 expression and survival. CONCLUSIONS: We conclude that uPA and MMP-9 are potential prognostic indicators in pancreatic cancer, whereas microvessel density may not be one. This study confirms our previous observation that uPA is made by the tumor cells themselves. Presence of uPA in vessels of tumor stroma suggests that uPA is in circulation, and its measurement and that of MMP-9 in the blood of these patients may aid in prognosis. Patients showing overexpression of uPA and MMP-9 have a trend toward shorter survival time.     

In situ gene expression of urokinase-type plasminogen activator and its receptor in transitional cell carcinoma of the human bladder

The urokinase-type plasminogen activator (uPA) system plays a central role in the blood clot dissolution and tissue plasticity. uPA is a serine protease that is also involved in the metastatic process upon activation and binding to its receptor (uPAR). Studies have shown that levels of uPA in malignant tumors are higher than in the corresponding normal tissue or in benign tumors of the same tissue. We investigated uPA and uPAR gene expression in 20 human transitional cell carcinomas (TCC) of the bladder (n=19) and the renal pelvis (n=1) in comparison with adjacent non-malignant tissues. We performed mRNA in situ hybridization (isH) and immunohistochemical staining. uPA-mRNA and uPAR-mRNA were present in 95% (19/20) and 85% (17/20) of the TCC samples, respectively and significantly higher expressed than in the adjacent normal tissue. uPA-mRNA was expressed only in malignant urothelial cells, whereas uPAR-mRNA was localized in malignant urothelial cells as well as in surrounding stromal cells. There was a statistically significant lower expression of uPA/uPAR-protein in adjacent normal tissue. Strong uPAR-protein signal intensity was related to a marked protein expression as semi-quantitatively determined by immunohistochemistry. For uPA-protein this observation was less frequent. There was a statistical trend that higher expression of uPA and uPAR corresponded with tumor stage and grade of TCC. Statistical significance was reached for uPAR-antigen compared to tumor stage (p=0.025). We conclude that higher expression of uPA and uPAR could indicate a more aggressive phenotype of TCC.     

Prognostic impact of stromal cell-derived urokinase-type plasminogen activator in gastric carcinoma

BACKGROUND: Urokinase-type plasminogen activator (uPA) plays an important role in the destruction of the extracellular matrix and basement membrane around cancer cells. In the current study, the authors investigated uPA expression in cancer cells and stromal cells in patients with gastric carcinoma. METHODS: uPA activity was determined by an enzymatic assay using synthetic substrate (S-2444) in tumor specimens obtained from 71 patients with gastric carcinoma and was compared with the results of immunohistochemical staining for uPA. RESULTS: Higher uPA activity was significantly associated with tumors with peritoneal metastases and tumors with deeper invasion into the gastric wall. Undifferentiated tumors showed significantly higher uPA activities compared with differentiated tumors. The 25 patients with high uPA activity (> or = 60 U/mg protein) had a lower survival rate than the 46 patients with low uPA activity (< 60 U/mg protein) (P < 0.05). uPA activity showed prognostic significance in patients with International Union Against Cancer Stage II and Stage III tumors (P < 0.05, respectively). There was no significant relation between immunohistochemical expression of uPA in cancer cells and uPA enzymatic activity. However, uPA expression in stromal cells significantly correlated with uPA activity in tumor tissues. The uPA expression in stromal cells also correlated with tumor histology and peritoneal metastases. CONCLUSIONS: These results suggest that uPA enzymatic activity is a prognostic factor in gastric carcinoma, and that uPA produced by stromal cells may regulate cancer cell invasion.     

Modulation of invasive properties of human glioblastoma cells stably expressing amino-terminal fragment of urokinase-type plasminogen activator

The binding of urokinase-type plasminogen activator (uPA) to its receptor (uPAR) on the surface of tumor cells is involved in the activation of proteolytic cascades responsible for the invasiveness of those cells. The diffuse, extensive infiltration of glioblastomas into the surrounding normal brain tissue is believed to rely on modifications of the proteolysis of extracellular matrix components; blocking the interaction between uPA and uPAR might be a suitable approach for inhibiting glioma tumorigenesis. We assessed how expression of an amino-terminal fragment (ATF) of uPA that contains binding site to uPAR affects the invasiveness of SNB19 human glioblastoma cells. SNB19 cells were transfected with an expression plasmid (pcDNA3-ATF) containing a cDNA sequence of ATF-uPA. The resulting ATF-uPA-expressing clones showed markedly less cell adhesion, spreading, and clonogenicity than did control cells. Endogenous ATF expression also significantly decreased the invasive capacity of transfected glioblastoma cells in Matrigel and spheroid-rat brain cell aggregate models. ATF-uPA transfectants were also markedly less invasive than parental SNB19 cells after injection into the brains of nude mice, suggesting that competitive inhibition of the uPA-uPAR interaction on SNB19 cells by means of transfection with ATF cDNA could be a useful therapeutic strategy for inhibiting tumor progression.     

uPA在三阴性乳腺癌组织中的表达及临床意义

目的:分析uPA在三阴性乳腺癌中的表达以及与临床病理特征的关系。方法:应用免疫组化方法检测23例三阴性乳腺癌、56例非三阴性乳腺癌及20例乳腺良性疾病标本中uPA的表达,并对其进行临床病理学分析。结果:uPA在三阴性乳腺癌、非三阴性乳腺癌和乳腺良性疾病组织中的阳性表达率分别为78.26%、55.36％和10.00%,统计结果显示具有显著统计学差异（P＜0.01）。23例三阴性乳腺癌患者中,腋窝淋巴结转移阳性组uPA阳性表达率为93.33%,而腋窝淋巴结转移阴性组为50.00%（P＜0.05）;组织学分组中,G1级组uPA阳性表达率为33.33%,G2级组为71.43%,G3级组为92.31%,阳性表达率随着分级的增加而逐渐升高,差异具有统计学意义（P＜0.05）。uPA表达与年龄和肿瘤大小无关。结论:uPA在三阴性乳腺癌中高表达,提示其可以作为三阴性乳腺癌预后不良的指标之一。