Mayo Medical School, Mayo Clinic, Rochester, MN 55905, USA.
Curr Oncol Rep. 2013 Jun;15(3):207-16. doi: 10.1007/s11912-013-0315-7.
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.
恶性胸腔积液(MPE)是癌症相关发病率的重要来源。每年,美国有超过 15 万名患者因 MPE 而呼吸困难,生活质量下降。目前的管理策略主要具有姑息价值,侧重于症状控制;它们不能解决胸腔积液的病理生物学问题,也不能提高生存率。进一步阐明病理生理学机制,并结合开发针对该过程的新型治疗方法,如针对胸腔内化疗药物,有可能极大地提高我们目前管理方案的疗效。血管内皮生长因子-A(VEGF-A)已被认为是恶性胸腔积液形成的关键细胞因子。肿瘤细胞、间皮细胞和浸润免疫细胞产生的高水平 VEGF 导致血管通透性增加、癌细胞迁移和血管生成。因此,贝伐单抗等抗血管生成疗法,一种针对 VEGF-A 的单克隆抗体,可能在恶性胸腔积液的治疗中有一定的作用。本文综述了恶性胸腔积液的发病机制和潜在治疗策略,重点关注血管生成和抗血管生成治疗。