Piperdi Bilal, Merla Amartej, Perez-Soler Roman
Montefiore Medical Center, 1300 Morris Park Avenue, Mazur Building, Room 616, Bronx, NY, 10461, USA,
Drugs. 2014 Mar;74(4):403-13. doi: 10.1007/s40265-014-0182-z.
Non-small cell lung cancer (NSCLC) is the most common type of lung cancer, and can be further classified as nonsquamous carcinoma (including adenocarcinoma, which accounts for 40 % of NSCLCs) and squamous NSCLC, which makes up 30 % of NSCLC cases. The emergence of inhibitors of epidermal growth factor receptors, anaplastic lymphoma kinase, and vascular endothelial growth factors (VEGF) in the last decade has resulted in steady improvement in clinical outcomes for patients with advanced lung adenocarcinoma. However, improvements in the survival of patients with squamous NSCLC have remained elusive, presenting an urgent need for understanding and investigating therapeutically relevant molecular targets, specifically in squamous NSCLC. Although anti-VEGF therapy has been studied in squamous NSCLC, progress has been slow, in part due to issues related to pulmonary hemorrhage. In addition to these safety concerns, several phase III trials that initially included patients with squamous NSCLC failed to demonstrate improved overall survival (primary endpoint) with the addition of antiangiogenic therapy to chemotherapy compared with chemotherapy alone. Angiogenesis is an established hallmark of tumor progression and metastasis, and the role of VEGF signaling in angiogenesis is well established. However, some studies suggest that, while inhibiting VEGF signaling may be beneficial, prolonged exposure to VEGF/VEGF receptor (VEGFR) inhibitors may allow tumor cells to utilize alternative angiogenic mechanisms and become resistant. As a result, agents that target multiple angiogenic pathways simultaneously are also under evaluation. This review focuses on current and investigational antiangiogenic targets in squamous NSCLC, including VEGF/VEGFRs, fibroblast growth factor receptors, platelet-derived growth factor receptors, and angiopoietin. Additionally, clinical trials investigating VEGF- and multi-targeted antiangiogenic therapies are discussed.
非小细胞肺癌(NSCLC)是最常见的肺癌类型,可进一步分为非鳞状癌(包括腺癌,占NSCLC的40%)和鳞状NSCLC,后者占NSCLC病例的30%。过去十年中,表皮生长因子受体、间变性淋巴瘤激酶和血管内皮生长因子(VEGF)抑制剂的出现,使晚期肺腺癌患者的临床结局稳步改善。然而,鳞状NSCLC患者生存率的提高仍然难以实现,迫切需要了解和研究与治疗相关的分子靶点,特别是在鳞状NSCLC中。尽管抗VEGF治疗已在鳞状NSCLC中进行研究,但进展缓慢,部分原因是与肺出血相关的问题。除了这些安全问题外,一些最初纳入鳞状NSCLC患者的III期试验未能证明,与单纯化疗相比,化疗联合抗血管生成治疗可提高总生存期(主要终点)。血管生成是肿瘤进展和转移的既定标志,VEGF信号在血管生成中的作用已得到充分证实。然而,一些研究表明,虽然抑制VEGF信号可能有益,但长期暴露于VEGF/VEGF受体(VEGFR)抑制剂可能会使肿瘤细胞利用替代血管生成机制并产生耐药性。因此,同时靶向多种血管生成途径的药物也在评估中。本综述重点关注鳞状NSCLC中当前和正在研究的抗血管生成靶点,包括VEGF/VEGFRs、成纤维细胞生长因子受体、血小板衍生生长因子受体和血管生成素。此外,还讨论了研究VEGF和多靶点抗血管生成治疗的临床试验。