Genentech, Inc., 1 DNA Way, South San Francisco, CA 94080, USA.
Cell. 2010 Apr 2;141(1):166-77. doi: 10.1016/j.cell.2010.01.033.
It has been recently reported that treatment with an anti-placenta growth factor (PlGF) antibody inhibits metastasis and primary tumor growth. Here we show that, although anti-PlGF treatment inhibited wound healing, extravasation of B16F10 cells, and growth of a tumor engineered to overexpress the PlGF receptor (VEGFR-1), neutralization of PlGF using four novel blocking antibodies had no significant effect on tumor angiogenesis in 15 models. Also, genetic ablation of the tyrosine kinase domain of VEGFR-1 in the host did not result in growth inhibition of the anti-VEGF-A sensitive or resistant tumors tested. Furthermore, combination of anti-PlGF with anti-VEGF-A antibodies did not result in greater antitumor efficacy than anti-VEGF-A monotherapy. In conclusion, our data argue against an important role of PlGF during primary tumor growth in most models and suggest that clinical evaluation of anti-PlGF antibodies may be challenging.
最近有报道称,抗胎盘生长因子(PlGF)抗体的治疗可抑制转移和原发性肿瘤生长。在这里,我们表明,尽管抗 PlGF 治疗抑制了伤口愈合、B16F10 细胞的渗出以及过表达 PlGF 受体(VEGFR-1)的肿瘤的生长,但使用四种新型阻断抗体中和 PlGF 对 15 种模型中的肿瘤血管生成没有显著影响。此外,在宿主中基因敲除 VEGFR-1 的酪氨酸激酶结构域也不会导致所测试的抗 VEGF-A 敏感或耐药肿瘤的生长抑制。此外,抗 PlGF 与抗 VEGF-A 抗体联合使用并未比抗 VEGF-A 单药治疗产生更大的抗肿瘤疗效。总之,我们的数据表明,在大多数模型中,PlGF 在原发性肿瘤生长过程中不起重要作用,并表明对抗 PlGF 抗体的临床评估可能具有挑战性。