Paulis Yvette W J, Soetekouw Patricia M M B, Verheul Henk M W, Tjan-Heijnen Vivianne C G, Griffioen Arjan W
Department of Internal Medicine, Division of Medical Oncology, School for Oncology and Developmental Biology (GROW), Maastricht University Medical Center, Maastricht, The Netherlands.
Biochim Biophys Acta. 2010 Aug;1806(1):18-28. doi: 10.1016/j.bbcan.2010.01.001. Epub 2010 Jan 14.
Solid tumour growth is dependent on the development of an adequate blood supply. For years, sprouting angiogenesis has been considered an exclusive mechanism of tumour vascularization. However, over the last years, several other mechanisms have been identified, including vessel-co-option, intussusception, recruitment of endothelial precursor cells (EPCs) and even mechanisms that do not involve endothelial cells, a process called vasculogenic mimicry (VM). The latter describes a mechanism by which highly aggressive tumour cells can form vessel-like structures themselves, by virtue of their high plasticity. VM has been observed in several tumour types and its occurrence is strongly associated with a poor prognosis. This review will focus on signalling molecules and cascades involved in VM. In addition, we will discuss the presence of VM in relation to ongoing cancer research. Finally, we describe the clinical significance of VM regarding anti-angiogenesis treatment modalities.
实体瘤的生长依赖于充足血液供应的形成。多年来，芽生血管生成一直被认为是肿瘤血管形成的唯一机制。然而，在过去几年中，人们发现了其他几种机制，包括血管共选、套叠式血管生成、内皮祖细胞（EPC）募集，甚至还有一些不涉及内皮细胞的机制，即所谓的血管生成拟态（VM）。后者描述了一种机制，即高侵袭性肿瘤细胞凭借其高度可塑性自身形成血管样结构。VM已在多种肿瘤类型中被观察到，其出现与预后不良密切相关。本综述将聚焦于参与VM的信号分子和信号级联反应。此外，我们将讨论VM在当前癌症研究中的存在情况。最后，我们阐述VM在抗血管生成治疗模式方面的临床意义。
