膀胱移行细胞癌患者血清骨形成蛋白-2和血管内皮生长因子水平变化

目的：检测骨形成蛋白-2和血管内皮生长因子水平在膀胱移行细胞癌患者血清中的水平。方法：采用ELISA法检测20例健康人、58例膀胱移行细胞癌患者术前的血清BMP-2和VEGF的含量,评价二者在膀胱移行细胞癌发生发展中的意义。结果：膀胱移行细胞癌患者血清中BMP-2和VEGF的水平明显高于健康人,并与肿瘤的浸润深度和分化程度及淋巴结转移、远处转移和临床病理分期密切相关（P〈0.05）,且两者存在明显相关性（P〈0.05）。结论：检测膀胱移行细胞癌患者血清中VEGF、BMP-2的水平,有助于临床诊疗和预后评估。     

大肠癌患者VEGF和Endostatin的表达及其与临床病理特征的关系

目的：探讨大肠癌患者手术前后血清血管内皮生长因子（VEGF）和Endostatin的动态变化规律及其与临床病理特征的关系。方法：ELISA法检测大肠癌患者（大肠癌组）术前及术后2周血清VEGF和Endostatin水平,并与大肠腺瘤患者（大肠腺瘤组）和健康对照者（对照组）进行比较。结果：1）大肠癌组术前血清VEGF水平显著高于大肠腺瘤组及对照组（P均〈0.01）。2）大肠癌组术前血清Endostatin水平显著高于大肠腺瘤组及对照组（P均〈0.01）。3）大肠癌组术前血清VEGF、Endostatin水平与原发肿瘤大小、细胞分化程度、区域淋巴结转移、肝转移及Dukes分期密切相关（P均〈0.05）,与性别、肿瘤部位等因素无关（P〉0.05）。4）大肠癌组术后2周血清VEGF水平较术前显著下降,而血清Endostatin水平较术前升高（P均〈0.01）。结论：大肠癌患者血清VEGF和Endostatin水平升高,且与原发肿瘤大小、细胞分化程度、区域淋巴结转移、肝脏转移及Dukes分期等因素有密切关系;血清VEGF和Endostatin水平是评价大肠癌恶性行为、预测浸润和转移程度的有效指标。     

血清VEGF、MCP-1联合LncRNA XIST评估膀胱癌患者预后的价值

目的 探讨血清血管内皮生长因子（VEGF）、单核细胞趋化蛋白-1（MCP-1）联合长链非编码核糖核酸 X染色体失活特异性转录本（LncRNA XIST）评估膀胱癌患者预后的价值。方法 选择2018年6月至2019年6月本院收治的膀胱癌患者52例作为观察组,另选择同期接受体检的健康者43例作为对照组。两组分别于术前和体检时采集空腹状态外周静脉血,测定血清VEGF、MCP-1、LncRNA XIST水平,并进行相关性分析。术后随访1年,记录术后6个月和1年生存率。根据受试者工作特征（ROC）曲线计算血清VEGF、MCP-1、LncRNA XIST预测膀胱癌患者生存的截断值,将患者分为VEGF、MCP-1、LncRNA XIST高表达组和低表达组,分析不同亚组患者的生存情况。结果 观察组的血清VEGF、MCP-1、LncRNA XIST水平显著高于对照组,差异均有统计学意义（均P<0.01）。VEGF表达水平与膀胱癌患者肿瘤最大直径、T分期、分化程度、肿瘤分级、局部肿瘤浸润深度、远处转移、淋巴转移有相关性（P<0.05）;MCP-1表达水平与膀胱癌患者T分期、分化程度、肿瘤分级、局部肿瘤浸润深度有相关性（P<0.05）;LncRNA XIST表达水平与膀胱癌患者T分期、分化程度、肿瘤分级、局部肿瘤浸润深度、淋巴转移有相关性（P<0.05）。血清VEGF、MCP-1联合LncRNA XIST检查对膀胱癌诊断及预后的评估价值均高于单项和双项检查（AUC=0.909,95%CI：0.850～0.968;AUC=0.682,95%CI：0.538～0.826）。VEGF、MCP-1和LncRNA XIST高表达组的膀胱癌患者术后1年生存率显著低于低表达组,差异有统计学意义（P<0.05）。结论 血清VEGF、MCP-1联合LncRNA XIST检测有助于提高膀胱癌患者诊断率,且对预后具有一定评估价值。     

吡柔比星灌注化疗对膀胱癌患者血液中血管生长内皮因子的影响

目的：探讨吡柔比星(THP)对膀胱癌患者血液中血管内皮生长因子(VEGF)的影响。方法：采用双抗体夹心ELISA法对21例膀胱癌患者及10例正常人血液中VEGF的检测，研究膀胱癌患者在THP化疗前、后和术后血液中VEGF的变化，以及不同分级和不同浸润程度的患者在化疗前、后血液中VEGF的表达。结果：THP的灌注化疗，能明显降低膀胱癌患者血液中的VEGF的水平。结论：THP能有效地杀死膀胱癌细胞，降低患者血液中VEGF的水平。     

膀胱移行细胞癌血清中肝细胞生长因子定量测定的临床预测价值

目的：探讨血清中肝细胞生长因子(HGF)测定在膀胱移行细胞癌(BTCC)诊断及随访中的价值。方法：采用酶联免疫测定(EIA)法定量测定45例BTCC患者血清中HGF含量，同时对10例BTCC术后复查阴性患者；9例癌前病变患者；11例其他泌尿系疾病患者；14例健康对照者进行检测。结果：①BTCC组血清中HGF含量显著高于其他组；②HGF含量随分期、分级增高而增加；③初、复发肿瘤间HGF含量差异无显著性意义。结论：BTCC血清中HGF含量明显升高并同肿瘤的侵袭状态密切相关，HGF可能成为一项有价值的用于BTCC筛选诊断和术后随诊的肿瘤标记物。     

胰岛素样生长因子I受体在膀胱移行细胞癌中的表达

目的研究胰岛素样生长因子Ⅰ受体(IGF-1R)在膀胱移行细胞癌中的表达及其与临床的关系。方法78例膀胱癌标本来自2000年~2002年间在我院手术治疗的膀胱移行上皮肿瘤患者,采用免疫组织化学法检测不同临床分期,病理分级患者以及初发及复发患者膀胱移行细胞癌组织的IGF-1R水平。结果在膀胱移行细胞癌中IGF-1R的表达阳性率明显升高,IGF-1R的表达与肿瘤的临床分期和病理分级以及肿瘤复发呈正相关(P<0.05)。结论IGF-1R在膀胱移行细胞癌的生长中起重要的作用,可以作为临床判断患者预后的辅助指标。     

血管内皮生长因子与肿瘤坏死因子α在膀胱肿瘤中的相关性

目的 研究血管内皮生长因子(vascular endothelial growth factor,VEGF)和肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)在膀胱尿路上皮肿瘤组织中的表达及其相关性和临床意义.方法 利用免疫组化技术分别对30例膀胱尿路上皮肿瘤和10例癌旁正常膀胱组织中VEGF和TNF-α的表达进行判定.结果 VEGF和TNF-α在膀胱尿路上皮肿瘤组织中的阳性表达显著高于癌旁正常组织.VEGF与膀胱尿路上皮肿瘤的病理分级和I临床分期均相关;TNF-α仅与膀胱尿路上皮肿瘤临床分期相关,与病理分级无关.两者在膀胱尿路上皮肿瘤中的表达呈正相关.结论 VEGF与TNF-α表达的相关性提示内源性TNF-α在膀胱肿瘤组织中可能参与VEGF介导的血管新生通路,从而促进膀胱肿瘤的生长.     

血清血管内皮生长因子、胰岛素样生长因子-1水平与胸腔镜食管癌根治术后食管胃吻合口漏的相关性研究

目的 探讨血清血管内皮生长因子(VEGF)、胰岛素样生长因子(IGF)-1水平与胸腔镜食管癌根治术后食管胃吻合口漏的关系。方法 2015年9月～2022年9月我院收治的食管癌病人425例,根据术后发生食管胃吻合口漏情况分为吻合口漏组(31例)和无吻合口漏组(394例)。检测血清VEGF、IGF-1水平,分析影响胸腔镜食管癌根治术后食管胃吻合口漏发生的危险因素以及VEGF、IGF-1预测术后食管胃吻合口漏发生的价值。结果 吻合口漏组术后血清VEGF、IGF-1水平降低,无吻合口漏组血清VEGF、IGF-1水平增高,吻合口漏组术前、术后1天、术后2天、术后3天血清VEGF、IGF-1水平均低于无吻合口漏组,差异有统计学意义(P<0.05)。术后肺部感染、低白蛋白、术后3天VEGF、术后3天IGF-1与术后食管胃吻合口漏有关(P<0.05)。术后3天VEGF、术后3天IGF-1水平预测术后食管胃吻合口漏的曲线下面积为0.675、0.655,联合两项指标曲线下面积为0.841,高于单独指标(Delong z=3.752、3.218,P<0.05)。结论 胸腔镜食管癌根治术后吻...     

淋巴管内皮生长因子-C在膀胱移行细胞癌中的表达及其临床意义

目的 :探讨具有促进淋巴管内皮细胞增殖和毛细淋巴管增生的淋巴管内皮生长因子 C(VEGF C)在膀胱移行细胞癌 (BTCC)中的表达及其与肿瘤淋巴管浸润、淋巴结转移等临床病理因素的关系。方法 :采用免疫组织化学方法研究 4 5例BTCC中VEGF C的表达水平 ,观察评估VEGF C的阳性表达与淋巴管浸润、淋巴结转移等临床病理资料的相关性。结果 :4 5例中 ,VEGF C阳性 36例 ,VEGF C的阳性表达与肿瘤分级、分期、静脉或淋巴管浸润、淋巴结及前列腺侵犯明显相关 (P <0 .0 5 ) ;多因素分析显示VEGF C的表达是唯一影响盆腔淋巴结转移的独立因素 (P =0 .0 0 3)。结论 :VEGF C与BTCC淋巴管浸润和转移有显著相关性 ,检测BTCC中VEGF C的表达能够预示盆腔淋巴结是否转移。     

膀胱癌血清中MMP-9与VEGF水平检测及意义

目的　检测基质金属蛋白酶 9(MMP 9)与血管内皮生长因子 (VEGF)在膀胱癌患者血清中的水平 ,探讨其与肿瘤的分级、分期的关系。　方法　采用sandwich ELISA法检测 5 8例膀胱癌患者血清中MMP 9和VEGF水平 ,正常对照组 4 5例。　结果　膀胱癌患者血清中MMP 9和VEGF的水平分别为 737 12 μg/L和 114 8 88ng/L ,均显著高于对照组 4 2 3 5 1μg/L和 84 6 96ng/L(P <0 0 1)。两者的水平与肿瘤的分级、分期有关 ,其中局部浸润性癌显著高于浅表性癌 (P <0 0 1) ;远处转移组显著高于局部浸润组 (P <0 0 1) ;而浅表性癌与对照组无差别 (P >0 0 5 )。G3 级患者MMP 9和VEGF水平均显著高于G1和G2 级 (P <0 0 1)。　结论　膀胱癌患者血清中MMP 9和VEGF水平显著升高 ,并与肿瘤的分级、分期及远处转移有关 ,提示检测两者血清水平有助于对膀胱癌恶性程度的判断。     

胰腺癌患者外周血促血管生成因子浓度与疾病进展的关系

目的探讨胰腺癌患者外周血促血管生成因子中血管内皮细胞生长因子（VEGF）、碱性成纤维细胞生长因子（bFGF）及类胰岛素生长因子（IGF-1）浓度与临床病理学特点之间的关系。方法酶联免疫吸附试验测定32例胰腺癌可切除患者,24例胰腺癌不可切除患者和20例健康人外周血的VEGF、bFGF及IGF-1浓度,分析其与胰腺癌患者性别、年龄、病理分级、肿瘤大小、有无淋巴结及远处转移、是否侵犯血管及临床分期的关系。结果胰腺癌患者VEGF及bFGF浓度显著高于健康人（P〈0．01）,IGF-1浓度差异无统计学意义（P〉0．05）;胰腺癌不可切除组较可切除组VEGF显著升高（P〈0．05）,bFGF及IGF浓度差异无统计学意义（P〉0．05）;VEGF与胰腺癌分化、淋巴结转移、血管侵袭、远处转移及临床分期相关;bFGF与肿瘤大小及肿瘤分化相关;IGF-1与血管侵袭相关。结论胰腺癌进展过程中特有的生物学特性与胰腺癌不同时期的血管形成调控密切相关,促血管生成因子对于胰腺癌的进展发挥至关重要的作用,检测外周血促血管生成因子的表达对于胰腺癌临床筛查、诊断及治疗可能具有重要意义。     

肝特异性胰岛素样生长因子-Ⅰ基因敲除鼠乳腺癌组织中基因变化及胰岛素样生长因子-Ⅰ对血管生成的影响

目的 探讨低血清胰岛素样生长因子-Ⅰ(IGF-Ⅰ)水平小鼠及正常水平小鼠乳腺癌模型中生长因子相关基因的变化及血管内皮细胞生长因子在乳腺癌组织中的表达与微血管密度的关系.方法 应用DMBA诱导肝脏特异性IGF-Ⅰ基因敲除鼠(LID鼠)及基因未敲除鼠(对照鼠)建立原发乳腺癌模型,基因芯片技术检测小鼠乳腺肿瘤及正常乳腺组织中相关基因的差异表达,免疫组织化学法检测其中VEGF表达及微血管密度.结果 LID鼠组肿瘤的发生时间、生长速度及大小均低于对照组(P＜0.05);(2)LID鼠组肿瘤组织的VEGF表达及MVD均弱于对照鼠组(P＜0.05);(3)LID鼠组肿瘤组织中基因IGF-Ⅰ、IGFBP-4、IGFBP-7较对照组上调,而基因IGF-Ⅱ,IGF-IIR、IGFBP-2、IGFBP-3、IGFBP-5下调.结论 IGF-Ⅰ促进小鼠乳腺癌的发生发展,且与血管生长密切相关.IGF-Ⅰ在肿瘤的发生、发展及转移中可能起重要作用.     

不同配方肠外营养对肝硬化大鼠生长激素/胰岛素样生长因子-1轴的影响

目的探讨不同配方肠外营养对肝硬化大鼠肝部分切除术后生长激素/胰岛素样生长因子-1轴的影响。方法正常大鼠作为对照组,肝硬化大鼠随机分为肝硬化术前组,肝硬化肝部分切除术后1 d组,术后行Novamin肠外营养5 d组,术后行Hepa肠外营养5 d组,各组n=6。测大鼠肝功能、血糖及血清GHI、GF-1I、GFBP-3水平,用RT-PCR法检测肝ALBmRNAI、GF-1 mRNA、IG-FBP-3mRNA的表达,肝组织行Ki67免疫组化染色。结果Hepa组肠外营养5 d后血清ALT、ALP、GH分别为(103±23)IU/L(、571±92)IU/L、(1.55±0.12)ng/ml,均比Novamin组明显降低,而血清IGF-1I、GFPB-3分别为(966.4±54.7)ng/ml(、6.9±0.2)ng/ml,均明显升高,肝ALBmRNA、IGF-1mRNAI、GFBP-3mRNA表达水平分别为(1.24±0.06)、(0.85±0.00)、(0.69±0.02),也明显升高,但肝Ki67指数(4.8%±0.3%vs 4.4%±0.4%)却无显著性差异。血清IGF-1I、GFPB-3与血清AST、ALT、ALP水平呈负相关,与血清ALB呈正相关。结论肝硬化大鼠不同配方肠外营养均可反映在生长激素/胰岛素样生长因子-1轴的变化,检测血清IGF-1,IGFBP-3水平有助于营养素的选择。     

Circulating VEGF levels in the serum of gastric cancer patients: correlation with pathological variables,patient survival,and tumor surgery

OBJECTIVE: To evaluate the clinical usefulness of serum vascular endothelial growth factor (VEGF) levels in gastric cancer patients. SUMMARY BACKGROUND DATA: Vascular endothelial growth factor plays an important role in the formation of new blood vessels involved in the growth and metastatic spread of solid tumors, but there is limited information regarding the clinical significance of serum VEGF levels in cancer patients. METHODS: Serum VEGF concentrations were measured by an enzyme linked immunosorbent assay in 61 healthy controls and in 58 gastric cancer patients before surgery, and then again at 7 and 30 days after surgery. The association between preoperative serum VEGF levels, clinicopathological features and patient survival, and their changes following surgery were evaluated. RESULTS: Serum VEGF levels in gastric cancer patients were significantly higher than those in controls. There was a significant association between serum VEGF levels and disease stage, as well as invasion depth of the tumor and the presence of distant metastases. Serum VEGF levels decreased significantly after radical resection of the primary tumor and increased in patients with unresectable tumors. Multivariate regression analysis showed that serum VEGF level is an independent prognostic factor for survival. CONCLUSIONS: Serum VEGF levels in gastric patients are significantly higher compared with normal controls and correlate with local tumor extent, disease stage, and the presence of distant metastases. Preoperative serum VEGF concentration decreases significantly after radical resection of the primary tumor and is an independent prognostic factor for patient survival suggesting that determination of serum VEGF levels may be clinically useful.     

Expression and significance of vascular endothelial growth factor receptor 2 in bladder cancer

PURPOSE: Vascular endothelial growth factor has a critical role in maintaining tumor microvasculature and, as such, is an attractive target for anti-angiogenic therapy. Aberrant expression of VEGF receptors, especially VEGFR2, on epithelial tumor cells allows VEGF to stimulate growth and migration of tumor cells in an autocrine and/or paracrine manner. Therefore, we studied the expression of VEGF and VEGFR2 in bladder cancer, and the relationship to disease characteristics. MATERIALS AND METHODS: Expression of VEGF and VEGFR2 was studied in a cohort of 72 patients with transitional cell cancer of the bladder. Tumor tissues from all patients were analyzed by immunohistochemistry and examined by a pathologist blinded to patient outcome. Patient demographics and disease outcome were correlated with expression of these markers. Bladder cancer cell lines that express VEGFR2 were studied in vitro and in vivo to establish the significance of VEGF/VEGFR2 signaling. RESULTS: Expression of VEGF and VEGFR2 was observed in 58% and 50% of urothelial tumor cells, respectively. VEGF expression failed to correlate with clinical variables. However, VEGFR2 expression correlated with disease stage (coefficient 0.23, p = 0.05). In addition, VEGFR2 expression increased with tumor invasion into the muscle (p <0.01). Experiments with VEGFR2 positive bladder cancer cell lines in vitro demonstrated increased invasion in response to VEGF. In addition, VEGF inhibition augmented the effect of docetaxel in a murine xenograft model of bladder cancer with a significant inhibition in proliferative index and microvascular density, and induction of apoptosis. CONCLUSIONS: Increased VEGFR2 expression correlates with several features that predict progression of urothelial cancer, including disease stage and invasive phenotype. VEGF targeted therapy may enhance the efficacy of standard therapy for bladder cancer.     

Association between the levels of serum inflammatory cytokines high-mobility group box-1, insulin-like growth factor-1, vascular endothelial growth factor 165 and progression of diabetic nephropathy

Objectives To determine the association between serum levels of high-mobility group box-1 (HMGB1), insulin-like growth factor-1 (IGF-1), vascular endothelial growth factor 165 (VEGF165) and occurrence and development of diabetic nephropathy (DN). Methods A total of 136 patients diagnosed as diabetic nephropathy (DN group) in Huai'an First People's Hospital between January 2016 to January 2018 were randomly selected in the study, including microalbuminuria group (n=62), macroalbuminuria group (n=50) and renal insufficiency group (n=24). Meanwhile, 115 healthy examiners during the same period were collected as normal control group. Serum glucose, serum total cholesterol (TC), serum triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C) and urinary albumin/urine creatinine ratio (UAlb/Cr) were detected in all subjects. Enzyme-linked immunosorbent assay (ELISA) was adopted to detect the serum concentrations of HMGB1, IGF-1 and VEGF165. Pearson correlation test was used to analyze the correlation between serum HMGB1, IGF-1 and VEGF165. Logistic ordered multi-classification regression was used to analyze the risk factors of DN progression, and the receiver operating characteristic curve (ROC) was drawn to evaluate the clinical predictive value of HMGB1, IGF-1 and VEGF165 in the progression of DN. Results The concentrations of serum HMGB1, IGF-1 and VEGF165 in DN patients were significantly higher than those in the control group (all P﹤0.05). There was a positive association between HMGB1 and IGF-1, HMGB1 and VEGF165, IGF-1 and VEGF165 (all P﹤0.01). Logistic regression analysis showed that elevated levels of HMGB1, IGF-1 and VEGF165 were independent risk factors for DN progression (OR=5.50, 1.05, 1.24, all P﹤0.05). The sensitivity, specificity and area under ROC curve of combined detection of HMGB1, IGF-1 and VEGF165 were higher than HMGB1, IGF-1 and VEGF165 alone (AUC=0.989, 0.984, 0.942, 0.878, P﹤0.05). Conclusions The serum levels of HMGB1, IGF-1 and VEGF165 are related to the severity of DN. The clinical predictive value of combined detection of HMGB1, IGF-1 and VEGF165 for DN progression is superior to that of single index detection of HMGB1, IGF-1 and VEGF165.