大肠腺瘤与非肿瘤性息肉中VEGF的表达差异及其与血管形成关系的研究

目的：探讨血管内皮生长因子（VEGF）在大肠腺瘤与非肿瘤性息肉中的表达差异及其与血管形成的关系。方法：采用免疫组化和原位杂交技术检测36例大肠腺瘤、36例非肿瘤性息肉、13例腺癌和11例正常黏膜组织中VEGF蛋白及其mRNA的表达，并计数微血管密度（MVD）。结果：大肠腺瘤组VEGF蛋白及其mRNA的表达和MVD值均高于非肿瘤性息肉组（P〈0．05）；大肠腺瘤组MVD值与VEGF的表达强度呈显著正相关（rs=0．640，P〈O．01）。结论：VEGF和血管形成密切相关，腺瘤的高表达和非肿瘤性息肉的低表达可能是两者恶变趋势差异的重要分子机理之一。     

人星形细胞瘤中eNOS和VEGF的表达与血管生成关系的研究

目的探讨内皮型一氧化氮合酶(eNOS)、血管内皮生长因子(VEGF)的表达与星形细胞瘤血管生成及恶性程度的相互关系.方法应用免疫组化方法检测37例星形细胞瘤和4例胶质增生组织eNOS、VEGF的表达水平,并检测Ⅷ因子相关抗原(FⅧRAg)以反映微血管密度.结果微血管密度随肿瘤恶性程度增高而显著增多(P＜0.05).eNOS、VEGF在血管内皮及肿瘤细胞胞质中均有表达,其阳性程度及标记指数(LI)均随血管密度及恶性程度增高而显著增高(P＜0.05).eNOS与VEGF的表达水平有明显的正相关性(P＜0.01).结论eNOS与VEGF可能相互影响促进肿瘤组织内血管生成,在星形细胞瘤的形成与发展过程中起着重要作用,其表达水平对判断恶性程度及预后有指导意义.     

Tumor markers in ovarian carcinoma.

This review analyzes in 2 ways the prognostic value of markers found in ovarian carcinomas before chemotherapy. It is known that neoangiogenesis, cyclooxygenase activity, and host responsiveness to chemotherapy can be evaluated by means of specific molecules recognized as tumor markers. However, host response as well as tumor histotype, grade of differentiation, clinical characteristics, and histopathologic characteristics must also be taken into account when selecting a treatment. Analysis must therefore focus on the molecular basis of aggressive disease, on tumor peculiarity, on the efficacy of chemotherapy, and on the host's response to the tumor. Although treatment may be more aggressive in patients with unfavorable prognostic elements, it may be modulated according to the molecular and cellular biology of the tumor and the host's response. When the tumor's molecular characterization contributes to the choice of treatment, prognostic markers may turn into predictive markers.     

ADENOVIRUS-MEDIATED EXPRESSION OF PEX, A NONCATALYTIC FRAGMENT OF MATRIX METALLOPROTEINASE-2, AND IT’S INHIBITION ON ANGIOGENESIS AND TUMOR GROWTH

Angiogenesis, the sprouting of new blood vessels from existing vessels, is a crucial process during embryogenesis, wound healing, and in the female reproductive organs[1]. A growing number of diseases,including cancer and inflammatory disorders, are characterized by excessive, de-regulated angiogenesis[2], attributable to increased production of growth factors or to decreased production of angiogenesis inhibitors[3]. Recently, a number of endogenous angiogenesis inhibitors have been identified…     

肝癌的血管生成与螺旋CT和动态MRI的强化

肝细胞癌(简称肝癌)是我国目前最常见的恶性肿瘤之一。新生血管生成是肝癌发生、生长过程中最重要的现象，血管形成的过程是肿瘤生长和转移所必需的阶段，并影响患者的预后。血管形成的过程对于理解肝癌在螺旋CT和动态MRI上的强化机理至关重要。肿瘤血管形成导致的影像学图像强化的改变也可以为肝癌的定性提供诊断依据，评价抗血管生成治疗的疗效，并预测肿瘤患者的预后。因此，本文综合肝癌新生血管的形成过程及进展，和它对螺旋CT和动态MRI强化的影响。进一步提高影像学对肿瘤的认识。     

血管内皮生长因子与肝癌肝动脉灌注化疗栓塞术

血管内皮生长因子在肝细胞肝癌血管生成的调控中起着关键性作用，经肝动脉灌注化疗栓塞术是不能手术肝癌患者最有效的姑息性治疗方法之一。本文从如下方面综述血管内皮生长因子肝癌肝动脉灌注化疗栓塞术的关系：①血管生成与血管内皮生长因子的关系；②血管内皮生长因子在肝癌中的表达；③肝癌的经肝动脉灌注化疗栓塞术治疗对血管内皮生长因子的影响；④抗血管生成策略与肝动脉灌注化疗栓塞术治疗的关系。     

CM101, a polysaccharide antitumor agent,does not inhibit wound healing in murine models

CM101 (previously called GBS toxin), a new anticancer polysaccharide that induces inflammatory reactions in neovasculature of tumors, does not cause similar reactions in neovasculature of healing wounds. It appears that treatment with CM101 will not interfere with normal wound healing in cancer patients.Abbreviations PVA polyvinyl alcohol - PBS phosphate-buffered saline     

人血管内皮生长因子D表达载体促进大鼠肝脏血管形成的研究

目的　人血管内皮生长因子D表达载体 (PCHO/hVEGF D)肠系膜上静脉注射后大鼠肝脏表达的维持时间以及血管形成效果观察。方法　健康级S D大鼠实验组 (2 4只 ) ,肠系膜上静脉注射PCHO/hVEGF D 15 0 μg/只 ,对照组 (18只 )同法注射等量生理盐水 ,然后行门静脉部分结扎术 ,制成门静脉高压症模型。术后 8、14、2 1d处死大鼠 ,取下肝脏标本 ,原位杂交法检测人血管内皮生长因子D(hVEGF D)mRNA的表达水平 ;Ⅷ因子法计算肝脏的血管计数。结果　实验 1、2、3组的hVEGF D的mRNA表达平均积分和阳性率分别为 6.83± 1.72 ,5 /6;3 .71± 2 .14 ,2 /7;2 .5 7± 2 .0 7,1/7;对照组极弱或无表达。第 1组与第 2组、第 3组的差异均有非常显著性 (t1/ 2 =2 .86,t1/ 3 =3 .99,P <0 .0 1)。第 2组和第 3组之间 ,差异无显著性 (t =1.0 16,P >0 .0 5 )。对照组未检测到表达。实验 1、2、3组的血管计数分别为 :12 .83± 4.0 2、8.2 0± 1.92 ,t =2 .3 5 ,P <0 .0 5 ;12 .71± 3 .14、8.80± 1.79,t =2 .49,P <0 .0 5 ;12 .0 0± 3 .74、7.67± 2 .5 0 ,t =2 .41,P <0 .0 5。 3组均显著高于相应对照组 ;实验组 3组之间血管计数差异无显著性。结论　裸基因肠系膜静脉注射PCHO/hVEGF D可以在门静脉部分结扎大鼠得到高效表达hVEGF D     

外源性透明质酸酶对人乳腺癌细胞侵袭力及血管形成能力的影响

目的　探讨外源性透明质酸酶(hyaluronidase, Hyase)对人乳腺癌细胞ZR 75 30 侵袭潜力及血管形成能力的影响。方法　通过建立体外侵袭模型和应用双室联合培养技术,观察外源性Hyase对ZR 75 30细胞穿透Matrigel(人工基底膜)的能力以及诱导血管内皮细胞形成血管能力的影响。结果　实验组的穿膜细胞数为(70.625±11.64)个,明显高于对照组的(22.125±6.09)个(P<0.01); 实验组的血管管腔数目为(34.5±2.4)条,明显高于对照组的(8.5±1.5)条(P<0.01)。结论　外源性Hyase有促进人乳腺癌细胞侵袭及诱导血管形成的作用。     

Complex congenital malformations and the impact of the plasminogen activator system and β-hCG in amniotic fluid

Objective

The plasminogen activator system and β-hCG may affect neural crest cells and angiogenesis, and thereby embryogenesis. Therefore, we investigated these parameters in amniotic fluids of pregnancies with a complex congenital malformation.

Study design

In a case-control study amniotic fluid samples were collected from 62 pregnancies with a complex congenital malformation and from 110 healthy control pregnancies at an obstetric department of a large university hospital in the Netherlands. We determined concentrations of tissue-type plasminogen activator (tPA), urokinase-type plasminogen activator (uPA), plasminogen activator inhibitors (PAI-1, PAI-2), tPA∼PAI-1 and uPA∼PAI-1 complexes, and β-hCG with enzyme-linked immunosorbent assays. Mann–Whitney U-tests and analysis of covariance, adjusting for gestational and maternal age, were performed for data comparisons.

Results

Compared with controls, cases demonstrated significantly lower adjusted geometric mean levels of uPA (24%), tPA (≥19%) and tPA∼PAI-1 (35%). Cases showed significantly higher adjusted mean levels of β-hCG (≥48%) and PAI-2 (10 ng/mL) than controls. Mean PAI-1 and uPA∼PAI-1 levels were comparable between both groups.

Conclusions

Disturbances in the plasminogen activator system and β-hCG levels are suggested to be involved in the pathogenesis of complex congenital malformations by affecting neural crest cell migration and angiogenesis.