Monzani Elena, La Porta Caterina Am
Molecular Oncology Laboratory, Department of Biomolecular Science and Biotechnology, University of Milan, 20133, Milan, Italy.
Stem Cell Rev. 2008 Spring;4(1):51-6. doi: 10.1007/s12015-008-9009-1.
Recently, many papers have shown that tumor vascularization can be explained by angiogenesis, recruitment, cooption, vasculogenic mimicry and by mosaic vessels. In particular, vasculogenic mimicry seems to be different from mosaic blood vessels, where tumor cells form a part of the surface of the vessel while the remaining part is covered by endothelium. In this case, tumor cells in apparent contact with the lumen do not show an endothelial phenotype. More recently, vasculogenic mimicry was proposed to occur in patients with multiple myeloma due to bone marrow macrophages. Herein, all these data are, for the first time, discussed critically in comparison to cancer stem cells-which show high trans-differentiative capacity-and bone-marrow derived stem cells. In fact, the presence of alternative vasculogenic patterns might be due to the presence of stem cell population (cancer stem cells or bone-marrow stem cells). In this connection, the literature is discussed extensively and possible models are proposed. Pharmacological perspectives will also discuss.
最近，许多论文表明，肿瘤血管生成可以通过血管生成、募集、血管生成拟态、血管生成拟态和镶嵌血管来解释。特别是，血管生成拟态似乎与镶嵌血管不同，在镶嵌血管中，肿瘤细胞构成血管表面的一部分，而其余部分则由内皮覆盖。在这种情况下，与管腔明显接触的肿瘤细胞不表现出内皮细胞表型。最近，有人提出由于骨髓巨噬细胞的存在，多发性骨髓瘤患者会发生血管生成拟态。在此，首次将所有这些数据与具有高转分化能力的癌症干细胞和骨髓来源的干细胞进行了批判性讨论。事实上，替代血管生成模式的存在可能是由于干细胞群体（癌症干细胞或骨髓干细胞）的存在。就此而言，对文献进行了广泛讨论并提出了可能的模型。还将讨论药理学观点。
