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肿瘤血管生成的起源。

The origins of vacularization in tumors.

机构信息

Department of Gastroenterology, Ruijin Hospital, Shanghai Jiaotong University, Shanghai, China.

出版信息

Front Biosci (Landmark Ed). 2012 Jun 1;17(7):2559-65. doi: 10.2741/4071.

DOI:10.2741/4071
PMID:22652798
Abstract

Vascularization is crucial for tumor growth and metastasis. Angiogenesis and vasculogenesis are widely accepted processes of tumor vascularization, particularly for endothelium-dependent vessels. In both these processes, the tumor vascular endothelial cells are derived from the host cells, including cells in normal tissues around the tumor or endothelial progenitor cells. In addition, the mosaic vessels occur as a transitional pattern between endothelium-dependent vessels and vasculogenic mimicry (VM), wherein both host endothelium and tumor cells participate in tumor vascularization. VM provides a special passage not involving endothelial cells and is conspicuously different from angiogenesis and vasculogenesis. The biological features of the tumor cells that form VM remain unknown. Tumor stem cells may participate in VM. In this review, we discuss the patterns involved in the origin of vascularization in tumors.

摘要

血管生成对于肿瘤的生长和转移至关重要。血管生成和血管发生是肿瘤血管生成的广泛接受的过程,特别是对于内皮依赖性血管。在这两个过程中,肿瘤血管内皮细胞来源于宿主细胞,包括肿瘤周围正常组织中的细胞或内皮祖细胞。此外,镶嵌血管是内皮依赖性血管和血管生成拟态(VM)之间的过渡模式,其中宿主内皮细胞和肿瘤细胞都参与肿瘤血管生成。VM 提供了一种不涉及内皮细胞的特殊通道,与血管生成和血管发生明显不同。形成 VM 的肿瘤细胞的生物学特征尚不清楚。肿瘤干细胞可能参与 VM。在这篇综述中,我们讨论了肿瘤血管生成起源的相关模式。

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Cell Prolif. 2025 Jun;58(6):e13814. doi: 10.1111/cpr.13814. Epub 2025 Jan 26.
2
Rhodocetin-αβ selectively breaks the endothelial barrier of the tumor vasculature in HT1080 fibrosarcoma and A431 epidermoid carcinoma tumor models.在HT1080纤维肉瘤和A431表皮样癌肿瘤模型中,罗多西汀-αβ可选择性破坏肿瘤脉管系统的内皮屏障。
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Collateral Damage Intended-Cancer-Associated Fibroblasts and Vasculature Are Potential Targets in Cancer Therapy.
有意的附带损伤——癌症相关成纤维细胞和脉管系统是癌症治疗的潜在靶点。
Int J Mol Sci. 2017 Nov 7;18(11):2355. doi: 10.3390/ijms18112355.
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Vascular Mimicry: A Novel Neovascularization Mechanism Driving Anti-Angiogenic Therapy (AAT) Resistance in Glioblastoma.血管拟态:一种驱动胶质母细胞瘤抗血管生成治疗(AAT)耐药的新型血管生成机制
Transl Oncol. 2017 Aug;10(4):650-660. doi: 10.1016/j.tranon.2017.04.007. Epub 2017 Jun 29.
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ETS transcription factors Etv2 and Fli1b are required for tumor angiogenesis.ETS转录因子Etv2和Fli1b是肿瘤血管生成所必需的。
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