Salgado R, Vermeulen P B, Benoy I, Weytjens R, Huget P, Van Marck E, Dirix L Y
Angiogenesis Group, Oncological Centre, A.Z. St.-Camillus/St.-Augustinus, Wilrijk-Antwerp, Belgium.
Br J Cancer. 1999 May;80(5-6):892-7. doi: 10.1038/sj.bjc.6690437.
We have compared the platelet number and the serum concentration of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and interleukin-6 (IL-6) in 80 blood samples of 50 patients with advanced cancer. We have also measured the mitogenic effect of patient sera on endothelial cells in vitro in order to estimate the biological activity of serum VEGF. Serum VEGF concentration correlated with platelet number (r = 0.61; P < 10(-4)). Serum IL-6 levels correlated with platelet count (r = 0.36; P < 10(-3)), with serum VEGF levels (r = 0.55; P < 10(-4)) and with the calculated load of VEGF per platelet (r = 0.4; P = 3 x 10(-4)). Patients with thrombocytosis had a median VEGF serum concentration which was 3.2 times higher (P < 10(-4)) and a median IL-6 serum level which was 5.8 times higher (P = 0.03) than in other patients. Serum bFGF did not show an association with any of the other parameters. Patient sera with high VEGF and bFGF content stimulated endothelial cell proliferation significantly more than other sera (P = 4 x 10(-3)). These results support the role of platelets in the storage of biologically active VEGF. Platelets seem to prevent circulating VEGF from inducing the development of new blood vessels except at sites where coagulation takes place. IL-6, besides its thrombopoietic effect, also seems to affect the amount of VEGF stored in the platelets. This is in accordance with the indirect angiogenic action of IL-6 reported previously. The interaction of IL-6 with the angiogenic pathways in cancer might explain the stimulation of tumour growth occasionally observed during IL-6 administration. It also conforms to the worse outcome associated with high IL-6 levels and with thrombocytosis in several tumour types and benign angiogenic diseases.
我们比较了50例晚期癌症患者80份血样中的血小板数量以及血管内皮生长因子(VEGF)、碱性成纤维细胞生长因子(bFGF)和白细胞介素-6(IL-6)的血清浓度。我们还在体外测量了患者血清对内皮细胞的促有丝分裂作用,以评估血清VEGF的生物活性。血清VEGF浓度与血小板数量相关(r = 0.61;P < 10⁻⁴)。血清IL-6水平与血小板计数相关(r = 0.36;P < 10⁻³),与血清VEGF水平相关(r = 0.55;P < 10⁻⁴),与计算得出的每个血小板的VEGF含量相关(r = 0.4;P = 3×10⁻⁴)。血小板增多症患者的VEGF血清浓度中位数比其他患者高3.2倍(P < 10⁻⁴),IL-6血清水平中位数比其他患者高5.8倍(P = 0.03)。血清bFGF与其他任何参数均无关联。VEGF和bFGF含量高的患者血清比其他血清更能显著刺激内皮细胞增殖(P = 4×10⁻³)。这些结果支持了血小板在储存生物活性VEGF中的作用。血小板似乎可防止循环中的VEGF诱导新血管生成,除非在发生凝血的部位。IL-6除了具有促血小板生成作用外,似乎还会影响血小板中储存的VEGF量。这与先前报道的IL-6的间接血管生成作用一致。IL-6与癌症血管生成途径的相互作用可能解释了在给予IL-6期间偶尔观察到的肿瘤生长刺激现象。这也符合在几种肿瘤类型和良性血管生成疾病中,高IL-6水平和血小板增多症与较差预后相关的情况。