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1.
目的: 利用7,12-二甲基苯蒽(DMBA)诱导的大鼠乳腺癌模型,探讨大豆苷元对乳腺癌肿瘤血管生成的抑制作用及机制。方法:建立DMBA诱导的乳腺癌大鼠模型,随机分为对照组、10、25、50和75 mg/kg大豆苷元灌胃组,观察各组肿瘤生长情况,测定肿瘤微血管密度(MVD),并计算各组肿瘤的增殖指数和凋亡指数;酶联免疫吸附试验(ELISA)法检测心脏离心血标本中血管内皮生长因子(VEGF)、碱性成纤维细胞生长因子(bFGF)和内皮抑素的水平。结果:与对照组比较,50和75 mg/kg大豆苷元组大鼠瘤体质量显著减轻(P<0.05),75 mg/kg大豆苷元组的凋亡指数增加,其抑制肿瘤血管生成的效果显著(P均<0.05)。与对照组比较,25、50和75 mg/kg大豆苷元组的VEGF水平降低,且呈剂量依赖性(P<0.05),同时50和75 mg/kg大豆苷元组的内皮抑素水平增加,差异均有统计学意义(P均<0.05)。结论:较高剂量(≥50 mg/kg)的大豆苷元能使大鼠乳腺肿瘤的微血管密度下降,可有效抑制乳腺肿瘤生长。  相似文献   

2.
目的 通过观察消癌平对体内小鼠移植瘤生长以及移植瘤肿瘤血管生成的影响,探讨消癌平抗肿瘤的机制。方法以C57BU6 雌性小鼠皮下接种构建Lewis 肺癌小鼠模型。造模1 周后,将45 只Lewis 肺癌小鼠随机分为A、B、C 3组,A 组给予顺铂(0.lmg/ml dl、d4、d7、dl0)作阳性对照,B 组给予消癌平注射液(5mg/ml dl~d21 ), C组予生理盐水(dl~d21)作阴性对照,均腹腔注射。治疗3 周后摘眼球取血,并处死动物,切除瘤体,称瘤重量并计算抑瘤率。应用免疫组化染色检测移植瘤组织中CD34 标记的微血管数目(MVD ) ,酶联免疫吸附试验(ELlSA)检测荷瘤小鼠血清中血管内皮生长因子(VEGF)和碱性成纤维细胞生长因子(bFGF)浓度。结果 消癌平组的抑瘤率15.69%、微血管密度(28.41±5. 985)个、血清VEGF (78.305±7.468) pg/ml 和bFGF (14.945 ±3.840) ng/ml,与生理盐水组比较,均有显著性差异(P<0.05)。结论消癌平注射液具有抗肿瘤血管生成和抑制肿瘤生长的作用,其机制可能通过降低Lewis 肺癌VEGF和bFGF的生成,从而降低肿瘤MVD, 抑制肿瘤血管生成及肿瘤生长。  相似文献   

3.
 目的 探讨槲皮素联合川芎嗪对小鼠Lewis肺癌生长的抑制作用及其机制。方法 复制C57BL小鼠Lewis肺癌模型,将40只接种Lewis肺癌的C57BL小鼠随机分成4组:对照组(A组)、槲皮素组(B组)、川芎嗪组(C组)、槲皮素+川芎嗪组(D组),每组10只。连续用药20日,观察移植瘤生长情况,于接种后第22天处死各组小鼠,采用免疫组化半定量检测肿瘤组织微血管密度(MVD)、血管内皮生长因子(VEGF)及增殖核抗原(PCNA)的表达水平,用原位凋亡TUNEL法检测肿瘤细胞凋亡指数(AI)。结果 (1)B、C、D组肿瘤的生长明显受到抑制,瘤重明显低于A组,其抑瘤率分剐为39.87%、35.45%、54.58%,D组抑瘤率明显高于B、C组,差异有显著性(P〈0.05)。(2)B、C、D组MVD、VEGF及PCNA表达水平明显低于A组(P〈0.05或0.01),尤其是D组表达最低。B、C、D组AI较A组增高(P〈0.05或0.01),D组最高。结论 槲皮素与川芎嗪联合用药可明显抑制Lewis肺癌移植瘤的生长,其作用机制与抑制微血管生成、抑制细胞增殖和促进细胞凋亡有关。  相似文献   

4.
目的:探讨姜黄素对二乙基亚硝胺( diethylnitrosamine, DEN)诱发大鼠肝细胞癌(hepatocellular carcinoma, HCC)缺氧后血管形成的影响。方法: 采用DEN诱发大鼠HCC,结扎肝动脉并构建大鼠HCC缺氧模型。将HCC模型大鼠按照数字表法随机分为单纯碘化油栓塞组(A组)、碘化油联合姜黄素栓塞组(B组)、碘化油联合肝周包膜组(C组)、碘化油联合姜黄素及肝周包膜组(D组),每组10 只。比较各组大鼠相应治疗后HCC细胞及组织VEGF、微血管密度(microvessel density,MVD)及大鼠中位生存时间(median survival time,MST)。结果:B组与D组的VEGF蛋白表达及MVD均比A组显著降低(P<0.01),而C组上述指标则与A组无显著变化(P>0.05)。B、C、D组比A组大鼠MST均显著延长(P<0.05),D组大鼠的MST高于B、C组(P<0.05)。结论:姜黄素可抑制HCC缺氧大鼠肿瘤血管的生成,可降低VEGF表达及MVD,起到延长大鼠生存期的作用。  相似文献   

5.
The aim of the present study was to detect the correlation between the expression of vascular endothelial growth factor (VEGF), angiopoietin 2 (Ang2), ephrinB2 and endocrine gland-derived vascular endothelial growth factor (EG-VEGF) and carcinogenesis or portal vein tumor thrombus (PVTT) formation in human hepatocellular carcinoma (HCC). The expression of VEGF, Ang2, ephrinB2 and EG-VEGF was detected by RT-PCR in 54 cases HCC without PVTT (group A), 9 cases HCC with PVTT (group B), 10 normal liver tissues (group D) and 10 cirrhosis tissues (group C). The samples were also stained with CD34 by immunohistochemistry. Quantitation of microvessel density (MVD) and semi-quantitation of VEGF, Ang2, ephrinB2 and EG-VEGF expression were analyzed to find the relations. The MVD was 146.69 +/- 77.79, 214.07 +/- 54.41, 32.85 +/- 8.49 and 34.83 +/- 8.29 in group A-D respectively with significant difference (F = 19.77, P = 0.000). The MVD in group A was higher than that in group C P = 0.006, but lower than that in group B P < or = 0.05 or 0.01. The expression levels of VEGF165, VEGF189, Ang2 and EG-VEGF mRNA were significantly different among the groups. The expression levels of VEGF165, Ang2 and EG-VEGF mRNA in group A were all higher than those in group C, but lower than those in group B P < 0.05 or 0.01. The MVD was significantly correlated with VEGF165, VEGF189, Ang2 and EG-VEGF mRNA with Spearman's related coefficient being 0.764, 0.510, 0.640 and 0.366 in HCC (P = 0.000, 0.000 0.000 and 0.003). In conclusion VEGF, Ang2 and EG-VEGF mRNA may play a role in angiogenesis and carcinogenesis of HCC. They can promote PVTT formation in HCC by modulating angiogenesis.  相似文献   

6.
We have previously reported that p53 mutations, loss of bax expression or decreased spontaneous tumor apoptosis were associated with poorer prognoses in maxillary sinus squamous cell carcinoma (SCC)(Cancer 94: 1968-1980, 2002). In the present study, we analyzed tumor angiogenesis monitored by expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and tumor microvessel density, in correlation with p53 status, spontaneous apoptosis or disease prognosis in the same group of 70 maxillary sinus SCC patients. Tumor biopsy specimens obtained prior to initiation of treatment were examined for expression of VEGF and bFGF and tumor microvessel density using immunohistological methods. Average vessel density (AVD) (range: 3-75; median: 25) and maximum vessel density (MVD) (range: 4-125; median: 53) were assessed by the number of microvessels stained with anti-CD31 mAb in tumor lesions. VEGF was expressed in 35 (50%) of 70 patients and bFGF was in 43 (61%). Patients with VEGF expression showed significantly higher levels of MVD than those without VEGF expression (57 vs. 38; P=0.019). The VEGF expression was observed more frequently in patients with p53 overexpression and/or mutation than in those with normal p53 status (P=0.048). The MVD inversely correlated with the apoptotic index (AI) defined as the number of single stranded (ss)-DNA-positive cells per 1000 tumor cells (r= -0.23; P=0.022). Patients with neck lymph node and/or distant metastases after surgery showed significantly higher levels of MVD than patients without any metastasis (64 vs. 42; P=0.048). Low histological effectiveness of radiochemotherapy correlated with bFGF expression (P=0.0059). To clarify actual prognostic factors for maxillary sinus SCC, we selected 57 patients treated uniformly with preoperative radiochemotherapy followed by maxillectomy. Kaplan-Meier analysis showed that survival was significantly worse in patients with high MVD (> or =80) than in those with low MVD (<80) (P=0.042). These data suggest that the VEGF expression in association with the p53 overexpression and/or mutations may cause increased microvascularity, decreased spontaneous apoptosis or metastases, while the bFGF expression may be associated with resistance to radiochemotherapy, thereby resulting in poorer prognoses in maxillary sinus SCC. VEGF and bFGF expression and tumor microvessel density in tumor lesions were analyzed in 70 patients with maxillary sinus squamous cell carcinoma. The VEGF expression dependent of p53 overexpression and/or mutations was associated with angiogenesis, decreased spontaneous tumor apoptosis and metastases, while the bFGF expression was associated with resistance to radiochemotherapy, resulting in poor prognosis.  相似文献   

7.
目的探讨尿纤溶酶原激活物(uPA)、血管内皮生长因子(VEGF)在食管癌中的表达及对肿瘤血管生成的影响。方法采用免疫组织化学sP法检测正常食管黏膜上皮组织(18例)及食管癌组织(68例)中uPA、VEGF的表达,检测CD。用以标记肿瘤微血管密度(MVD),根据MVD均值分为高、低MVD组,分析食管癌uPA、VEGF的表达和临床病理特征的关系及对肿瘤血管形成的影响。结果uPA蛋白在正常食管黏膜上皮组织、食管癌组织中的阳性率分别为27.8%(5/18)和70.6%(48/68),差异有统计学意义(X^2=11.63,P〈0.05);VEGF蛋白在正常食管黏膜上皮组织、食管癌组织中的阳性率分别为22.2%(4/18)和63.2%(43/68),差异有统计学意义(X^2=9.78,P〈0.05)。食管癌组织中uPA与VEGF表达有一致性(X^2=9.72,P〈0.05)。MVD平均为42.38±11.62,高MVD组uPA、VEGF蛋白表达显著高于低MVD组(X^2值分别为6.13和10.12,均P〈0.05)。uPA、VEGF蛋白表达与年龄、性别、病理类型无关(均P〉0.05),均与临床病理分期、分化程度和淋巴结转移相关(P〈0.05)。结论食管癌组织中uPA、VEGF蛋白高表达,可能促进肿瘤血管形成,提示预后不良。  相似文献   

8.
It has been demonstrated that vascular endothelial growth factor (VEGF) is associated with tumor progression as an angiogenic factor in esophageal squamous cell carcinoma (SCC)s. However, the role of other angiogenic factors such as transforming growth factor-alpha (TGF-alpha), platelet-derived endothelial cell growth factor (PD-ECGF), and basic fibroblast growth factor (bFGF) are still unknown in esophageal SCCs. In this study, we detected the expression of VEGF, TGF-alpha, PD-ECGF and bFGF in tissue specimens from 96 patients with SCC of the esophagus by immunohistochemical staining. To evaluate angiogenesis, endothelial cells were stained immunohistochemically and microvessel density (MVD) was counted in 24 cases. The positive rates for VEGF, TGF-alpha, PD-ECGF and bFGF were 65% (62/96), 67% (64/96), 66% (63/96), and 49% (47/96), respectively. Only TGF-alpha expression had a strong correlation with the average MVD (p=0.0059). However, the MVD increased as the number of positive factors for these 4 factors increased (p=0.0023). The expression of all of these factors significantly correlated to the depth of tumor invasion, and lymph node metastasis. Finally, survival analysis of the patients revealed that VEGF, TGF-alpha, and PD-ECGF were significant prognostic factors. However, multivariate analysis revealed that these factors were not prognostic. Thus, we suggest that TGF-alpha as well as VEGF, PD-ECGF and bFGF may be associated with angiogenesis, and the progression and metastasis of esophageal squamous cell carcinoma.  相似文献   

9.
目的建立乳腺非典型增生病动物模型,探讨非典型增生与血管生成的关系。方法采用灌服二甲基苯蒽+颈部枷具方法复制大鼠肝郁血瘀型乳腺非典型增生动物模型,并给予中药乳复汤治疗。常规染色观察大鼠乳腺组织病理组织形态,免疫组化方法检测MVD、VEGF和bFGF的表达。结果病证模型组乳腺非典型增生率90%,较单纯造模组高,P=0·0415;中药乳复汤治疗组非典型增生率较病证模型组低,P=0·0459;随着一般增生到非典型增生程度加重,MVD计数增多,VEGF、bFGF的表达升高,P<0·05。结论病证结合造模更适合中医动物实验要求,中药乳复汤具有抑制血管生成作用。  相似文献   

10.
Qi SY 《癌症》2003,22(3):320-323
背景与目的:血管生成是实体肿瘤生长、侵袭、扩散转移的关键,微血管密度(microvesselofdensity,MVD)可反映肿瘤的血管形成情况。血管内皮生长因子(vascularendothelialgrowthfactor,VEGF)是具有重要意义的促血管生长因子,它与肿瘤的生长密切相关。本研究检测卵巢交界性肿瘤组织中VEGF的表达和MVD,探讨它们与临床病理特征及预后的关系。方法:采用免疫组化SP法和原位杂交技术检测69例卵巢交界性肿瘤、18例卵巢良性肿瘤和27例卵巢恶性肿瘤组织中VEGF蛋白及VEGFmRNA的表达,用FⅧ因子单克隆抗体标记新生血管内皮,计数并计算MVD。结果:VEGF蛋白、VEGFmRNA在卵巢交界性肿瘤组织中的表达均介于卵巢良性肿瘤与卵巢恶性肿瘤之间,其结果差异均有显著性(P<0.05);也与卵巢交界性肿瘤的临床分期、MVD值密切相关(P<0.05);但VEGF与卵巢交界性肿瘤的组织分型、有无腹腔种植无关(P>0.05)。结论:VEGF与卵巢肿瘤的生长、侵袭、转移密切相关;检测VEGF有助于判断卵巢肿瘤的恶性程度,为判断卵巢交界性肿瘤患者的预后提供依据。  相似文献   

11.
目的探讨蜂毒素对人肝癌裸鼠移植瘤生长的影响及其抗血管生成作用。方法建立人肝癌裸鼠皮下移植瘤模型,观察蜂毒素对肿瘤生长的影响。采用免疫组织化学法,检测肿瘤组织微血管密度(microvessel density,MVD)及碱性成纤维细胞生长因子(basic fibroblast growth factor,bFGF)、缺氧诱导因子-1α(hypoxia inducible factor-1α,HIF-1α)和核转录因子κB(nuclear factorκB,NF-κB)的水平。结果蜂毒素低、中、高剂量组相对肿瘤增殖率分别为48.78%、38.33%和33.82%。与生理盐水组比较,蜂毒素处理组肿瘤体积明显缩小(P〈0.01)。免疫组化结果显示,蜂毒素可降低肿瘤组织MVD,且蜂毒素处理组bFGF、HIF-1α和NF-κB蛋白水平明显低于生理盐水组(P〈0.01)。结论蜂毒素可抑制裸鼠皮下移植瘤的生长,其作用机制可能是降低NF-κB活性,抑制HIF-1α转录,进而下调bFGF表达,最终阻碍肝癌血管生成。  相似文献   

12.
The effects of dietary supplementation of flavonol quercetin on both 7,12-dimethylbenz(a)anthracene (DMBA)- and N-nitrosomethylurea-induced mammary cancer in female Sprague-Dawley rats were determined. Quercetin diet was started 1 wk before intragastric instillation of DMBA (65 mg/kg of body weight) or i.v. injection of N-nitrosomethylurea (50 mg/kg of body weight) and was continued during the entire period (20 wk) of the experiment. Dietary quercetin inhibited both the incidence and the number of palpable rat mammary tumors; rats fed on 2% quercetin had 25% less incidence of mammary cancer, while the average number of mammary tumors per rat was reduced by 39% at 20 wk post-DMBA administration compared to animals on a control diet. In a separate experiment, a 5% quercetin diet elicited a greater inhibitory effect on the induction of rat mammary tumors by DMBA than was observed with a 2% quercetin diet. The inhibitory effect of quercetin on mammary tumor incidence in rats on 2% and 5% diets and on tumor multiplicity in animals on a 5% diet was statistically significant (P less than 0.05). In addition, the risk of the development of a palpable tumor (as determined by the nonparametric estimate of the hazard function) in the quercetin-fed group was lower than the group on control diet throughout the course of the experiment. Furthermore, 5% dietary quercetin significantly inhibited (P less than 0.05), although to a lesser extent than observed in DMBA-induced tumor formation, both the incidence and the number of palpable mammary tumors per rat induced by N-nitrosomethylurea. Dietary quercetin did not elicit any detectable sign of toxicity. The gain in body weight in rats on the quercetin diet and the quantity of diet consumed per rat per week were similar to those for rats on the control diet.  相似文献   

13.
Angiogenesis plays an important role in tumor growth, metastasis, and prognosis. Vascular endothelial growth factor (VEGF) is a potent endothelial mitogen and acts on the angiogenic stimulation of human neoplasias. In infiltrative ductal carcinoma (IDC), VEGF expression is correlated with high vascularity. Tumor-associated macrophages (TAMs) contribute to tumor proliferation, progression and angiogenesis and have a complex role in tumor biology. In this study, the correlations between microvessel density (MVD), VEGF expression, and TAMs and their relations to clinicopathological parameters such as tumor size, metastatic lymph node, mitotic activity index (MAI) and tumor grade were investigated in 48 cases of IDC and 30 infiltrative lobular carcinoma (ILC) cases. MVD showed a significant positive correlation with TAMs, VEGF, metastatic lymph nodes, tumor size and grade in IDC (P < 0.001). In ILC, MVD and tumor size were positively correlated (P = 0.003), while MVD was not correlated with VEGF, TAMs, MAI, metastatic lymph nodes, and grade. These findings are suggestive of angiogenesis stimulation in IDCs by VEGF, driving the macrophages into the tumor area. MVD and TAMs were found to be important prognostic factors in IDCs. On the other hand, however, VEGF did not contribute to angiogenesis in ILCs, and MVD and TAMs did not have any prognostic significance. These results suggest the involvement of factors not related to VEGF in the angiogenesis of lobular carcinoma.  相似文献   

14.
目的:探讨低剂量紫杉醇联合沙利度胺对小鼠S-180肉瘤血管生成的作用。方法:建立S-180移植瘤小鼠模型,将40只荷瘤小鼠随机分为4组。A组:生理盐水组(对照组);B组:紫杉醇组,腹腔内注射20 mg/kg,每周3次,连续2周;C组:沙利度胺组,200 mg/kg灌胃,每周3次,连续2周;D组:紫杉醇+沙利度胺组,腹腔内注射紫杉醇(20 mg/kg)和沙利度胺(200 mg/kg)灌胃,每周3次,连续2周。观察瘤重、抑瘤率、血管内皮生长因子(vascular endothelial growth factor,VEGF)的表达和微血管密度(microvessel density,MVD)计数。结果:与对照组比较,B、C、D组均能降低瘤重、减少VEGF的表达、降低MVD计数(P<0.05);D组分别与B、C组比较,VEGF的表达及MVD计数均低于B、C组,且差异具有统计学意义(P<0.05)。结论:小剂量紫杉醇联合沙利度胺能一定程度上抑制S180肉瘤血管的生长,两者具有协同作用。  相似文献   

15.
Survivin is involved in multiple signaling mechanisms in tumor maintenance, and accumulated studies elucidate that knockdown of survivin in endothelial cells could inhibit angiogenesis; however, the role of survivin in tumor cells to regulate tumor-derived angiogenesis remains largely unclear. In the present study 80 cases of brain glioma were chosen and protein expressions of survivin, vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and platelet-derived growth factor (PDGF) in glioma cells were investigated by immunohistochemistry (IHC). Human umbilical vein endothelial cells (HUVEC) were cocultured with human glioma U251 wild-type cells, U251 cells survivin silenced, SHG44 wild-type cells, and SHG44 survivin-overexpressing cells, respectively. The proliferation and migration of HUVEC were evaluated by MTT assay and transwell chamber assay. The microvessels density (MVD) marked by CD31 expression in vascular endothelial cells in glioma xenografts in nude mice was detected by IHC. VEGF, bFGF, and PDGF in the aforementioned cells were detected by quantitive PCR (qPCR), Western blot, ELISA, and IHC in vitro and in vivo. The results showed that VEGF immunoreactivity score (IRS), bFGF IRS, and PDGF IRS were all positively correlated with survivin IRS in gliomas, respectively (P < 0.01). Survivin in human glioma cells could significantly promote the proliferation and migration of HUVEC and increase MVD, which could be contributed to survivin-dependent burst of VEGF and bFGF expression, followed by increase of tumor growth and proliferation. In summary, survivin, through upregulation of VEGF and bFGF, plays an essential role during glioma angiogenesis.  相似文献   

16.
Objective: To explore the mechanism and significance of tumor angiogenesis by observing changes of microvesseldensity (MVD) and expression of vascular endothelial growth factor (VEGF) in residual tumor tissuesafter cryoablation. Materials and Methods: A total of 18 nude mice xenograft models with transplanted lungadenocarcinoma cell line A549 were established and randomly divided into 3 groups when the maximum diameterof tumor reached 1 cm: control, cisplatin (DDP) and cryoablation. The nude mice were sacrificed after 21-dcryoablation to obtain the tumor tissues. Then immunohistochemistry was applied to determine MVD and theexpression of VEGF in tumor tissues. Results: The tumor volumes of control group, DDP group and cryoablationgroup were 1.48±0.14 cm3, 1.03±0.12 cm3 and 0.99±0.06 cm3 respectively and the differences were significant(P<0.01), whereas MVD values were 21.1±0.86, 24.7±0.72 and 29.2±0.96 (P<0.01) and the positive expressionrates of VEGF were 36.2±1.72%, 39.0±1.79% and 50.8±2.14% (P<0.01), respectively, showing that MVD wasproportional to the positive expression of VEGF (r=0.928, P<0.01). Conclusions: Cryoablation can effectivelyinhibit tumor growth, but tumor angiogenesis significantly increases in residual tumors, with high expressionof VEGF playing an important role in the residual tumor angiogenesis.  相似文献   

17.
VEGF、bFGF和ER在子宫内膜癌的表达   总被引:19,自引:1,他引:18  
目的探讨血管内皮细胞生长因子(VEGF)的表达与子宫内膜癌临床病理参数和预后的关系,以及其与雌激素受体(ER)和碱性成纤维细胞生长因子(bFGF)表达之间的关系。方法采用免疫组化SP法检测66例子宫内膜癌和19例正常子宫内膜的石蜡切片VEGF、ER和bFGF的表达。结果子宫内膜癌VEGF的阳性表达率为80.3%,其表达与组织学分级呈正相关(r=0.4021,P<0.01);ER表达与组织学分级呈负相关(r=-0.2455,P<0.05);VEGF与bFGF的表达呈正相关(r=0.2939,P<0.05)。ER阴性表达比ER阳性表达的患者预后差(P<0.05)。ER表达与VEGF和bFGF的表达无显著相关性。结论VEGF是子宫内膜癌重要的血管生成因子,ER表达与子宫内膜癌的预后有关,但与bFGF和VEGF的表达无关。  相似文献   

18.
19.
腋淋巴结阴性乳腺癌新生血管形成活性的研究   总被引:2,自引:0,他引:2  
Li HJ  Jing J  Zhao YB  Zhu JQ  Zhang SY  Shi ZD 《癌症》2002,21(1):75-78
背景与目的:观察腋淋巴结阴性乳腺癌血管内皮细胞生长因子(vascular endothelial growth factor,VEGF)的表达和微血管密度(microvessel density,MVD)的分布,并探讨VEGF和MVD与肿瘤大小(T)、组织学分级、雌激素受体水平(ER)、及复发转移的关系,同时评价检测VEGF和MVD对预后预测的价值。方法:用Ⅷ因子抗体与抗VEGF多克隆抗体分别对62例腋淋巴结阴性乳腺癌作病理切片的免疫组织化学染色,在显微镜下判断VEGF染色程度以及进行微血管计数。随访预后情况。结果:MVD和VEGF与组织学分级和复发转移有关(P<0.05)。VEGF表达阳性患者和高MVD患者的总生存率和无瘤生存率均明显低于VEGF表达阴性患和低MVD患者的相应生存率(P<0.01)。尤其在VEGF表达阳性且MVD也高的患者更明显(P<0.005)。VEGF和MVD之间也明显相关(P<0.01)。结论:VEGF与MVD与腋淋巴结阴性乳腺癌患者的预后相关,均可作为有价值的预后预测指标,两者联合应用对预后判断更有价值。VEGF是促进肿瘤新生血管形成的重要因素。  相似文献   

20.
目的:观察化疗栓塞治疗前后原发性肝癌患者血液中血管生成调节因子(VEGF和bFGF)表达水平的变化,探讨术后肿瘤血管生成情况。方法:采用双抗体夹心EHSA法检测人血清VEGF、bFGF含量,比较化疗栓塞治疗前后的表达水平。结果:11例肝癌患者血液中VEGF和bFGF的表达水平介入后均较介入前明显升高,(P〈0.05)。两者表达呈正相关(P=0.012)。结论:化疗栓塞治疗促进了血液中VEGF和bFGF表达;VEGF和bFGF的表达在一定程度上反映了化疗栓塞术后肿瘤血管生成状况。  相似文献   

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