Denekamp J
CRC Gray Laboratory, Mount Vernon Hospital, Northwood, Middlesex, UK.
Cancer Metastasis Rev. 1990 Nov;9(3):267-82. doi: 10.1007/BF00046365.
The blood supply to all solid tumours consists of parasitized normal vessels and new vessels which have been induced to grow by the presence of the tumour. These vessels are inadequate in many respects, being tortuous, thin-walled, chaotically arranged, lacking innervation and with no predetermined direction of flow. The walls consist of a basement membrane lined with rapidly proliferating immature endothelial cells, and are more permeable than normal vessels. The spacing of the vessels and their average diameters are not optimal for nutrient provision. This paper focuses on the evidence that many existing therapies may already have, as part of their action, a vascular mediated process of killing tumour cells. This may result from local changes within individual vessels or from systemic alterations in blood pressure, viscosity, coagulability etc. The hallmarks of vascular injury are identified and the dangers of discarding useful anticancer agent by failing to understand their mechanism of action are highlighted.
所有实体肿瘤的血液供应都由受肿瘤影响的正常血管和因肿瘤存在而诱导生成的新血管组成。这些血管在很多方面存在不足,它们迂曲、壁薄、排列混乱、缺乏神经支配且没有预定的血流方向。血管壁由衬有快速增殖的未成熟内皮细胞的基底膜组成,并且比正常血管更具渗透性。血管的间距及其平均直径对于营养供应并非最佳状态。本文着重探讨的证据是,许多现有疗法可能已经在其作用过程中包含了一种血管介导的杀死肿瘤细胞的过程。这可能源于单个血管内的局部变化,或者血压、粘度、凝血性等的全身改变。确定了血管损伤的特征,并强调了因未能理解有用抗癌药物的作用机制而摒弃它们的危险性。