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首页> 外文期刊>Therapeutic advances in gastroenterology. >Tryptase mast cell density, protease-activated receptor-2 microvascular density, and classical microvascular density evaluation in gastric cancer patients undergoing surgery: possible translational relevance
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Tryptase mast cell density, protease-activated receptor-2 microvascular density, and classical microvascular density evaluation in gastric cancer patients undergoing surgery: possible translational relevance

机译:胃癌手术中胰蛋白酶的肥大细胞密度,蛋白酶激活的受体2微血管密度和经典微血管密度评估:可能的翻译相关性

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Mast cells (MCs) can stimulate angiogenesis, releasing several proangiogenic cytokines stored in their cytoplasm. In particular, MCs can release tryptase, a potent in vivo and in vitro proangiogenic factor via protease-activated receptor-2 (PAR-2) activation and mitogen-activated protein kinase (MAPK) phosphorylation. Nevertheless, no data are available concerning the relationship among tryptase MC density (TMCD), endothelial cells (ECs) positive to PAR-2 microvascular density (PAR-2-MVD) and classical MVD (C-MVD) in gastric cancer (GC) angiogenesis. In this study, we analyzed the correlation of TMCD, PAR-2-MVD, C-MVD with each other and with the main clinicopathological features in GC patients who underwent surgery. A series of 77 GC patients with stage T2-3N2-3M0 (classified by the American Joint Committee on Cancer for Gastric Cancer, 7th edition) were selected and then underwent surgery. Tumour tissue samples were evaluated by mean of immunohistochemistry and image analysis methods in terms of numbers of TMCD, PAR-2-MVD and C-MVD. A significant correlation between the TMCD, PAR-2-MVD and C-MVD groups with each other was found by Pearson t-test analysis (r ranged from 0.64 to 0.76; p value ranged from 0.02 to 0.03). There was no other significant correlation between the above parameters and clinicopathological features. Our in vivo preliminary data suggest that TMCD and PAR-2-MVD may play a role in GC angiogenesis and they could be further evaluated as a target of antiangiogenic therapy.
机译:肥大细胞(MCs)可以刺激血管生成,释放储存在其细胞质中的几种促血管生成细胞因子。特别是,MCs可以通过蛋白酶激活的受体2(PAR-2)激活和有丝分裂原激活的蛋白激酶(MAPK)磷酸化作用释放类胰蛋白酶,一种有效的体内和体外促血管生成因子。然而,尚无有关胃癌(GC)中类胰蛋白酶MC密度(TMCD),对PAR-2微血管密度(PAR-2-MVD)呈阳性的内皮细胞(EC)和经典MVD(C-MVD)之间关系的数据。血管生成。在这项研究中,我们分析了进行手术的GC患者中TMCD,PAR-2-MVD,C-MVD的相互关系以及主要临床病理特征。一系列77例GC患者,其T 2-3 N 2-3 M 0 期(由美国胃癌联合委员会分类)选择第7版《癌症》,然后进行手术。通过免疫组织化学和图像分析方法,根据TMCD,PAR-2-MVD和C-MVD的数量评估肿瘤组织样品。通过Pearson t检验分析发现TMCD,PAR-2-MVD和C-MVD组之间存在显着相关性(r介于0.64至0.76; p值介于0.02至0.03之间)。上述参数与临床病理特征之间没有其他显着相关性。我们的体内初步数据表明,TMCD和PAR-2-MVD可能在GC血管生成中起作用,它们可以进一步评估为抗血管生成治疗的靶标。

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