抗血管内皮生长因子治疗因 c-Met 抑制而复兴，但 c-Met 是否是答案？
Anti-VEGF therapy revived by c-Met inhibition, but is c-Met the answer?
机构信息
Department of Pharmacology, Division of Surgical Oncology, UT Southwestern Medical Center, Dallas, TX 75390-8593, USA.
出版信息
Cancer Discov. 2012 Mar;2(3):211-3. doi: 10.1158/2159-8290.CD-12-0037.
Abstract
A new study by Sennino and colleagues demonstrates that selective VEGF inhibition via the use of an anti-VEGF antibody is sufficient to increase invasion and metastasis in a c-Met-dependent manner. Anti-VEGF therapy induced tumor hypoxia, hypoxia-inducible factor 1α, and c-Met activation in the RIP-Tag2 model of neuroendocrine pancreatic cancer. Selective c-Met inhibition was sufficient to block these effects, providing a potential mechanism for and solution to overcome increased invasion in the face of anti-VEGF therapy.
摘要
新的研究表明，塞尼诺及其同事通过使用抗血管内皮生长因子抗体对血管内皮生长因子进行选择性抑制，足以通过 c-Met 依赖性方式增加侵袭和转移。抗血管内皮生长因子治疗会在神经内分泌胰腺癌细胞的 RIP-Tag2 模型中引起肿瘤缺氧、缺氧诱导因子 1α 和 c-Met 激活。选择性 c-Met 抑制足以阻断这些作用，为克服抗血管内皮生长因子治疗中侵袭增加提供了一种潜在机制和解决方案。
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本文引用的文献
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