肝癌抗血管生成治疗耐药的关键机制:血管共生

The key mechanism underlying resistance to anti-angiogenic therapy in liver cancer:vessel co-option

实体瘤的生长需要血液供应,而诱导新血管生成是实体肿瘤生长的必要条件。在此理论基础上,肿瘤抗血管生成治疗应运而生。尽管肝癌被认为是一种高度血管生成型肿瘤,但抗血管生成药物的疗效远未达到预期。近年来,血管共生作为一种长期存在,但被忽视的非血管生成型肿瘤血管化机制逐渐受到关注。血管共生为肿瘤组织可以通过“劫持”癌旁组织中已存在的血管,而非诱导血管生成以促进自身肿瘤生长。血管共生存在于多种肿瘤原发灶及转移灶,其被认为是介导抗血管生成治疗耐药的重要机制。笔者回顾肝癌中血管共生的证据、临床预后及分子机制,探讨血管共生在肝癌抗血管生成治疗耐药及其他抗肿瘤治疗策略中潜在的作用及意义。

The growth of solid tumors rely on angiogenesis to establish blood supply,and inducing neovascularization is a necessary condition for the growth of solid tumors.Anti-angiogenic therapies have been developed for tumors based on this theory.Although liver cancer is considered as a highly angiogenic tumor,the effectiveness of these drugs in anti-angiogenic therapies on liver cancer has not met expectations.In recent years,vessel co-option,as a long-standing but overlooked mechanism of vascularization of non-angiogenic tumors,has gradually attracted attention.Tumor tissue can promote its own growth by"hijacking"existing blood vessels in the para-carcinoma tissue instead of inducing angiogenesis,known as vessel co-option or vascular hijacking.Vessel co-option has been observed in a variety of tumors,both primary and metastatic,and is believed to be a key mechanism of anti-angiogenic resistance.The authors systematically examine the evidence,clinical prognosis,and molecular mechanisms of vessel co-option in liver cancer,and discuss its potential role in anti-angiogenic therapeutic resistance and alternative anti-tumor strategies for liver cancer.