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Evolving role of Sorafenib in the management of hepatocellular carcinoma 被引量:5
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作者 Ioannis A Ziogas Georgios Tsoulfas 《World Journal of Clinical Oncology》 CAS 2017年第3期203-213,共11页
Hepatocellular carcinoma(HCC) is one of the most common malignant diseases worldwide and comes third in cancer-related mortality.Although there is a broad spectrum of treatment options to choose from,only a few patien... Hepatocellular carcinoma(HCC) is one of the most common malignant diseases worldwide and comes third in cancer-related mortality.Although there is a broad spectrum of treatment options to choose from,only a few patients are eligible candidates to receive a curative therapy according to their stage of disease,and thus palliative treatment is implemented in the majority of the patients suffering from liver cancer.Sorafenib,a multikinase inhibitor,is the only currently approved agent for systemic therapy in patients with advanced stage HCC and early stage liver disease.It has been shown to improve the overall survival,but with various side effects,while its cost is not negligible.Sorafenib has been in the market for a decade and has set the stage for personalized targeted therapy.Its role during this time has ranged from monotherapy to neoadjuvant and adjuvant treatment with surgical resection,liver transplantation and chemoembolization or even in combination with other chemotherapeutic agents.In this review our aim is to highlight in depth the current position of Sorafenib in the armamentarium against HCC and how that has evolved over time in its use either as a single agent or in combination with other therapies. 展开更多
关键词 SORAFENIB Hepatocellular carcinoma LIVER NEOPLASM Multikinase inhibitor Targeted THERAPY tumor angiogenesis Signaling pathways ADJUVANT THERAPY LIVER cancer LIVER transplantation LIVER RESECTION
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CANSTATIN, A ENDOGENOUS INHIBITOR OF ANGIOGENESIS AND TUMOR GROWTH 被引量:2
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作者 苏影 朱建思 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2004年第3期229-234,共6页
Canstatin is a novel inhibitor of angiogenesis and tumor growth, derived from the C-terminal globular non-collageneous (NCl) domain of the a2 chain of type IV collagen. It inhibits endothelial cell proliferation and m... Canstatin is a novel inhibitor of angiogenesis and tumor growth, derived from the C-terminal globular non-collageneous (NCl) domain of the a2 chain of type IV collagen. It inhibits endothelial cell proliferation and migration in a dose-dependent manner, and induces endothelial cell apoptosis. In vivo experiments show that canstatin significantly inhibits solid tumor growth. The canstatin mediated inhibition of tumor is related to apoptosis. Canstatin- induced apoptosis is associated with phosphatidylinositol 3-kinase/Akt inhibition and is dependend upon signaling events transduced trough membrane death receptor. 展开更多
关键词 CANSTATIN Death receptor (DR) FLIP AKT inhibitor of tumor angiogenesis
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癌抑素Canstatin的抗肿瘤作用及其机制 被引量:1
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作者 苏影 朱建思 《肿瘤学杂志》 CAS 2004年第5期353-356,共4页
Canstatin是一种来源于Ⅳ型胶原α2链非胶原(NC1)区的血管生成和肿瘤生长抑制因子。它能剂量依赖性抑制血管内皮细胞增殖和迁移,诱导内皮细胞凋亡,在体内实验中Canstatin显著抑制实体瘤的生长。Canstatin的抗肿瘤作用可能与诱导凋亡有关... Canstatin是一种来源于Ⅳ型胶原α2链非胶原(NC1)区的血管生成和肿瘤生长抑制因子。它能剂量依赖性抑制血管内皮细胞增殖和迁移,诱导内皮细胞凋亡,在体内实验中Canstatin显著抑制实体瘤的生长。Canstatin的抗肿瘤作用可能与诱导凋亡有关,其作用机制在于抑制磷脂酰肌醇3鄄激酶/Akt(PI3鄄k/Akt)信号通路,并依赖膜死亡受体介导的信号事件。 展开更多
关键词 CANSTATIN 死亡受体 FLIP AKT 肿瘤血管牛成抑制剂
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TFPI-2、VEGF在非小细胞肺癌中的表达及相关性研究 被引量:5
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作者 董永强 梁江水 +4 位作者 殷桂林 朱水波 张晓明 纪涛 徐家行 《临床肺科杂志》 2013年第9期1625-1627,共3页
目的研究组织因子途径抑制物-2(tissue factor pathway inhibitor-2,TFPI-2)、血管内皮生长因子(vascular endotheli-al growth factor,VEGF)在非小细胞肺癌(non-small cell lung cancer,NSCLC)中的表达及其间的相关性。方法采用免疫组... 目的研究组织因子途径抑制物-2(tissue factor pathway inhibitor-2,TFPI-2)、血管内皮生长因子(vascular endotheli-al growth factor,VEGF)在非小细胞肺癌(non-small cell lung cancer,NSCLC)中的表达及其间的相关性。方法采用免疫组化法检测60例NSCLC组织TFPI-2、VEGF的表达及CD31单克隆抗体标记的微血管密度(MVD)。结果 NSCLC中临床分期为Ⅰ、Ⅱ、Ⅲ期的患者中TFPI-2表达阳性率分别为75.8%、25.0%和40.0%(P=0.003),无淋巴结转移和有淋巴结转移的患者中TF-PI-2表达阳性率分别为66.7%、38.1%(P=0.033)。临床分期为Ⅰ、Ⅱ、Ⅲ期的患者中EVGF表达阳性率分别为60.6%、88.3%和93.3%(P=0.040),无淋巴结转移和有淋巴结转移的患者中VEGF表达阳性率分别为64.1%、90.5%(P=0.028)。NSCLC组织中的TFPI-2的表达与VEGF的表达呈负相关(r=-0.351),差异有统计学意义(P=0.004)。高、低MVD组中的TFPI-2阳性表达率分别为41.2%、76.9%(P=0.006)。高、低MVD组中的VEGF阳性表达率分别为76.5%、30.87%(P=0.000)。结论 NSCLC中TFPI-2可能通过下调VEGF的表达抑制肿瘤新生血管的形成,从而抑制NSCLC的生长、浸润及转移。 展开更多
关键词 组织因子途径抑制物-2 血管内皮生长因子 肿瘤血管生成 非小细胞肺癌
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基质金属蛋白酶-9及基质金属蛋白酶组织抑制物-1与卵巢上皮性癌血管生成的关系 被引量:2
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作者 孙丽君 《中国妇幼保健》 CAS 北大核心 2009年第5期646-648,共3页
目的:探讨基质金属蛋白酶-9(MMP-9)及基质金属蛋白酶组织抑制物-1(TIMP-1)在卵巢上皮性癌血管生成中的作用。方法:采用免疫组织化学SP法检测45例卵巢上皮性癌组织中MMP-9和TIMP-1的表达,并检测其中微血管密度(MVD,CD34标记)。结果:卵巢... 目的:探讨基质金属蛋白酶-9(MMP-9)及基质金属蛋白酶组织抑制物-1(TIMP-1)在卵巢上皮性癌血管生成中的作用。方法:采用免疫组织化学SP法检测45例卵巢上皮性癌组织中MMP-9和TIMP-1的表达,并检测其中微血管密度(MVD,CD34标记)。结果:卵巢癌组织和卵巢良性肿瘤中MMP-9阳性表达率明显高于正常卵巢组织(P<0.01),而TIMP-1未见升高(P>0.05),并且TIMP-1在卵巢癌组织中的阳性表达率显著低于MMP-9(P<0.01)。MMP-9在卵巢癌组织中表达与MVD显著正相关(r=0.286,P<0.05),而TIMP-1与MVD无相关性(r=0.194,P>0.05)。卵巢癌中MMP-9表达高于TIMP-1者,其MVD显著高于MMP-9表达低于TIMP-1者(P<0.05)。结论:MMP-9和TIMP-1表达失衡可能在卵巢上皮性癌血管生成中起重要作用,MMP-9表达增强而TIMP-1表达降低,其血管生成能力可能显著增强,但并非唯一决定因素。检测卵巢上皮性癌中MMP-9和TIMP-1表达对进一步了解卵巢上皮性癌局部血管生成情况有一定应用价值。 展开更多
关键词 卵巢上皮性癌 基质金属蛋白酶 基质金属蛋白酶组织抑制物 肿瘤血管生成 微血管密度
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