Although blocking vascular endothelial growth factor (VEGF) signaling is clinically beneficial in certain cancers, tumor regrowth in treated patients suggests that compensatory angiogenic programs may limit the efficacy of anti-VEGF treatment. We found that association of galectin-1 with complex N-glycans on VEGFR2 links tumor hypoxia to VEGFR2 signaling and preserves angiogenesis in response to VEGF blockade.

中文翻译：

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将肿瘤缺氧与 VEGFR2 信号传导和补偿性血管生成联系起来：聚糖发挥作用。

尽管阻断血管内皮生长因子 (VEGF) 信号传导在某些癌症中具有临床益处，但接受治疗的患者的肿瘤再生长表明补偿性血管生成程序可能会限制抗 VEGF 治疗的疗效。我们发现半乳糖凝集素-1 与 VEGFR2 上的复杂 N-聚糖的关联将肿瘤缺氧与 VEGFR2 信号传导联系起来，并保留血管生成以响应 VEGF 阻断。