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The role of vascular endothelial growth factor in the pathogenesis, diagnosis and treatment of malignant pleural effusion

机译:血管内皮生长因子在恶性胸腔积液的发病机制,诊断和治疗中的作用

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摘要

Malignant pleural effusions (MPEs) are a significant source of cancer-related morbidity. Over 150,000 patients in the United States suffer from breathlessness and diminished quality of life due to MPE each year. Current management strategies are of mostly palliative value and focus on symptom control; they do not address the pathobiology of the effusion, nor do they improve survival. Further elucidation of the pathophysiological mechanisms, coupled with the development of novel treatments such as intrapleural chemotherapeutics targeting this process, has the potential to greatly improve the efficacy of our current management options. Vascular endothelial growth factor-A (VEGF-A) has been implicated as a critical cytokine in the formation of malignant pleural effusions. Elevated levels of VEGF produced by tumor cells, mesothelial cells, and infiltrating immune cells result in increased vascular permeability, cancer cell transmigration, and angiogenesis. Therefore antiangiogenic therapies such as Bevacizumab, a monoclonal antibody targeting VEGF-A, may have a potential role in the management of malignant pleural effusions. Herein we review the pathogenesis and potential treatment strategies of malignant pleural effusions, with a focus on angiogenesis and antiangiogenic therapeutics.
机译:恶性胸腔积液(MPE)是与癌症相关的发病率的重要来源。每年,由于MPE,超过150,000名患者患有呼吸困难和生活质量下降。当前的治疗策略主要具有姑息治疗价值,并且集中在症状控制上。他们没有解决积液的病理生物学问题,也没有提高生存率。进一步阐明其病理生理机制,以及开发针对该过程的新型疗法(例如胸膜内化疗剂),有可能极大地提高我们当前管理方案的功效。血管内皮生长因子-A(VEGF-A)被认为是恶性胸腔积液形成中的关键细胞因子。肿瘤细胞,间皮细胞和浸润性免疫细胞产生的VEGF水平升高,导致血管通透性增加,癌细胞迁移和血管生成。因此,抗血管生成疗法,例如贝伐单抗,一种靶向VEGF-A的单克隆抗体,可能在恶性胸腔积液的治疗中具有潜在作用。在本文中,我们回顾了恶性胸腔积液的发病机制和潜在的治疗策略,重点是血管生成和抗血管生成疗法。

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