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抗血管生成抑制剂的癌症联合疗法:全面综述。

Cancer combination therapies by angiogenesis inhibitors; a comprehensive review.

机构信息

Department of Pharmaceutics, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj, Kingdom of Saudi Arabia.

Institute of Pharmacy, Sechenov First Moscow State Medical University, 8 Trubetskaya St., bldg. 2, Moscow, 119991, Russian Federation.

出版信息

Cell Commun Signal. 2022 Apr 7;20(1):49. doi: 10.1186/s12964-022-00838-y.

DOI:10.1186/s12964-022-00838-y
PMID:35392964
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8991477/
Abstract

Abnormal vasculature is one of the most conspicuous traits of tumor tissue, largely contributing to tumor immune evasion. The deregulation mainly arises from the potentiated pro-angiogenic factors secretion and can also target immune cells' biological events, such as migration and activation. Owing to this fact, angiogenesis blockade therapy was established to fight cancer by eliminating the nutrient and oxygen supply to the malignant cells by impairing the vascular network. Given the dominant role of vascular-endothelium growth factor (VEGF) in the angiogenesis process, the well-known anti-angiogenic agents mainly depend on the targeting of its actions. However, cancer cells mainly show resistance to anti-angiogenic agents by several mechanisms, and also potentiated local invasiveness and also distant metastasis have been observed following their administration. Herein, we will focus on clinical developments of angiogenesis blockade therapy, more particular, in combination with other conventional treatments, such as immunotherapy, chemoradiotherapy, targeted therapy, and also cancer vaccines. Video abstract.

摘要

异常的血管生成是肿瘤组织最显著的特征之一,在很大程度上促进了肿瘤的免疫逃逸。这种失调主要源于促血管生成因子的分泌增强,也可以针对免疫细胞的生物事件,如迁移和激活。鉴于这一事实,血管生成阻断疗法通过破坏血管网络来消除恶性细胞的营养和氧气供应,从而建立起来以对抗癌症。鉴于血管内皮生长因子 (VEGF) 在血管生成过程中的主导作用,众所周知的抗血管生成药物主要依赖于靶向其作用。然而,癌细胞主要通过几种机制对抗血管生成药物产生耐药性,并且在给予这些药物后也观察到局部侵袭性增强和远处转移。在此,我们将重点介绍血管生成阻断疗法的临床进展,特别是与其他常规治疗方法(如免疫疗法、放化疗、靶向治疗和癌症疫苗)相结合的进展。视频摘要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdfb/8991477/41c7d0da2c3f/12964_2022_838_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdfb/8991477/d7d91717eafd/12964_2022_838_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdfb/8991477/f2fde319803c/12964_2022_838_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdfb/8991477/41c7d0da2c3f/12964_2022_838_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdfb/8991477/d7d91717eafd/12964_2022_838_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdfb/8991477/f2fde319803c/12964_2022_838_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdfb/8991477/41c7d0da2c3f/12964_2022_838_Fig3_HTML.jpg

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