There were high hopes for the new antiangiogenic medicament, bevacizumab, which could inhibit the creation of new blood vessels through binding to isoform A of vascular endothelial growth factor (VEGF). However, it is not only blood vessels that are responsible for tumor cell spread. During the process of tumor growth, lymphangiogenesis is mediated by other members of the VEGF family, specifically VEGF-C and VEGF-D, which act independent to bevacizumab. Therefore, based on the mechanism of bevacizumab action and the processes of angio- and lymphangiogenesis, we formed three hypotheses: (1) if the lymph nodes in primary ovarian cancers are metastatic, the outcome of bevacizumab treatment is worsened; (2) concerning the second-line treatment, bevacizumab will act in a weakened manner if recurrence occurs in lymph nodes as opposed to a local recurrence; (3) patients treated by bevacizumab are more likely to have recurrences in lymph nodes. These hypotheses raise the issue of the existing knowledge gap, which concerns the effect of bevacizumab on metastatic lymph nodes.
新型抗血管生成药物贝伐珠单抗曾备受瞩目，其通过结合血管内皮生长因子（VEGF）亚型A抑制新生血管形成。然而，肿瘤细胞扩散并非仅由血管系统介导。在肿瘤生长过程中，淋巴管生成由VEGF家族其他成员（特别是VEGF-C和VEGF-D）调控，这些因子不受贝伐珠单抗影响。基于贝伐珠单抗的作用机制及血管/淋巴管生成过程，我们提出三项假设：（1）若原发性卵巢癌存在淋巴结转移，贝伐珠单抗治疗效果将恶化；（2）在二线治疗中，相较于局部复发，淋巴结复发时贝伐珠单抗疗效将减弱；（3）接受贝伐珠单抗治疗的患者更易出现淋巴结复发。这些假设揭示了当前认知空白：贝伐珠单抗对转移性淋巴结的具体影响机制尚未明确。
肿瘤(癌症)患者之家