The key mechanism underlying resistance to anti-angiogenic therapy in liver cancer: vessel co-option
10.3760/cma.j.cn115610-20230908-00077
- VernacularTitle:肝癌抗血管生成治疗耐药的关键机制：血管共生
- Author:
Dan YANG
1
;
Xiangming DING
;
Dongxiao LI
;
Shumin DANG
;
Yujin PAN
;
Xiuling LI
;
Deyu LI
Author Information
1. 郑州大学人民医院消化内科，郑州 450003
- Keywords:
Liver neoplasms;
Vessel co-option;
Angiogenesis;
Anti-angiogenic therapy;
Drug resistance
- From:
Chinese Journal of Digestive Surgery
2023;22(S1):112-116
- CountryChina
- Language:Chinese
-
Abstract:
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.
