Pinedo H M, Verheul H M, D'Amato R J, Folkman J
Department of Medical Oncology, Academic Hospital Vrije Universiteit, Amsterdam, The Netherlands.
Lancet. 1998 Nov 28;352(9142):1775-7. doi: 10.1016/s0140-6736(98)05095-8.
Preclinical and clinical research show that tumour growth is dependent on angiogenesis. Activation of the coagulation cascade is commonly found in patients with cancer. We propose that platelets contribute to tumour-induced angiogenesis. The basis of our hypothesis is that platelets are a rich source of stimulators and inhibitors of angiogenesis and their interaction with the endothelium. Presumably, the antithrombotic state of normal endothelium is disturbed by endothelial stimuli derived from tumour cells. This hypothesis may explain the suggested clinical benefits of anticoagulants in cancer and implies that targeting of platelet interaction with tumour vasculature will inhibit angiogenesis.
临床前和临床研究表明，肿瘤生长依赖于血管生成。凝血级联反应的激活在癌症患者中普遍存在。我们提出，血小板有助于肿瘤诱导的血管生成。我们这一假设的依据是，血小板是血管生成刺激物和抑制剂的丰富来源，以及它们与内皮细胞的相互作用。据推测，正常内皮细胞的抗血栓状态会受到肿瘤细胞衍生的内皮刺激的干扰。这一假设可能解释了抗凝剂在癌症治疗中所显示的临床益处，并意味着针对血小板与肿瘤脉管系统的相互作用将抑制血管生成。
