期刊文献+

贝伐珠单抗治疗恶性腹腔积液的研究进展 被引量:4

Progression of bevacizumab in the treatment of malignant ascites
下载PDF
导出
摘要 恶性腹腔积液是晚期肿瘤患者常见的并发症,不仅严重影响患者的生活质量,还提示预后较差。目前针对恶性腹腔积液的全身治疗有限盐利尿、补充白蛋白、治疗原发肿瘤等,还有在此基础上进行腹腔穿刺引流及腹腔药物灌注等局部治疗。血管内皮生长因子(VEGF)是恶性腹腔积液形成的关键介质,其主要通过调节血管生成,增加血管通透性来诱导腹腔积液的形成。贝伐珠单抗是重组的人源化抗VEGF单克隆抗体,可与内源性VEGF竞争性结合VEGF受体(VEGFR),达到抑制肿瘤新生血管生成、减少腹腔积液形成、延缓肿瘤进展速度的作用。近年来有较多研究探索了贝伐珠单抗治疗恶性腹腔积液的临床应用方法、治疗疗效以及相关不良反应,本文现对这一领域的新进展作一综述。 Malignant ascites is one of the common complications of advanced tumors,which not only seriously affects the quality of life in patients with tumors,but also indicates a poor prognosis.At present,the main management is to treat malignant ascites the locally on the basis of systemic treatment of primary tumor,including puncture drainage,and intracavitary perfusion therapy and so on.Vascular endothelial growth factor(VEGF)is a key mediator in the formation of malignant ascites,mainly by regulating angiogenesis and increasing vascular permeability to induce the formation of peritoneal effusions.Bevacizumab is a recombinant humanized anti-VEGF monoclonal antibody,which competes with endogenous VEGF to bind to the vascular endothelial growth factor receptor(VEGFR)to inhibit tumor angiogenesis,hinder the formation of malignant ascites and slow down the rate of tumor progression.In recent years,a number of studies have explored the clinical applications,efficacy and adverse effects of bevacizumab in the treatment of malignant ascites.This review aims to summarizes the new progress in this field.
作者 陈嘉楠 丁文龙 朱思遥 姜子瑜 刘静冰 李灵常 CHEN Jianan;DING Wenlong;ZHU Siyao;JIANG Ziyu;LIU Jingbing;LI Lingchang(Department of Oncology, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine,Nanjing 210028,China)
出处 《临床肿瘤学杂志》 CAS 2022年第2期172-177,共6页 Chinese Clinical Oncology
基金 国家自然科学基金面上项目(81973525) 希思科-2019年度齐鲁肿瘤研究基金资助项目(Y-QL2019-0325)。
关键词 恶性腹腔积液 VEGF 贝伐珠单抗 Malignant ascites Vascular endothelial growth factor(VEGF) Bevacizumab
  • 相关文献

参考文献19

二级参考文献182

共引文献198

同被引文献51

引证文献4

二级引证文献12

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部