Nooijen P T, Manusama E R, Eggermont A M, Schalkwijk L, Stavast J, Marquet R L, de Waal R M, Ruiter D J
Department of Pathology, University Hospital Nijmegen, The Netherlands.
Br J Cancer. 1996 Dec;74(12):1908-15. doi: 10.1038/bjc.1996.652.
Isolated limb perfusion (ILP) with tumour necrosis factor alpha (TNF-alpha) and melphalan has shown impressive results in patients with irresectable soft tissue sarcomas and stage III melanoma of the extremities. The mechanisms of the reported in vivo synergistic anti-tumour effects of TNF-alpha and melphalan are not precisely understood. We have developed an ILP model in the rat using a non-immunogenic sarcoma in which similar in vivo synergy is observed. The aim of this present study was to analyse the morphological substrate for this synergistic response of TNF-alpha in combination with melphalan to shed more light on the pathomechanisms involved. Histology of the tumours from saline- (n = 14) and melphalan-treated (n = 11) rats revealed apparently vital tumour cells in over 80% of the cross-sections. Interstitial oedema and coagulation necrosis were observed in the remaining part of the tumour. Haemorrhage was virtually absent. TNF-alpha (n = 22) induced marked oedema, hyperaemia, vascular congestion, extravasation of erythrocytes and haemorrhagic necrosis (20-60% of the cross-sections). Oedema and haemorrhage suggested drastic alterations of permeability and integrity of the microvasculature. Using light and electron-microscopy, we observed that haemorrhage preceded generalised platelet aggregation. Therefore, we suggest that the observed platelet aggregation was the result of the microvascular damage rather than its initiator. Remarkably, these events hardly influenced tumour growth. However, perfusion with the combination of TNF-alpha and melphalan (n = 24) showed more extensive haemorrhagic necrosis (80-90% of the cross-sections) and revealed a prolonged remission (mean 11 days) in comparison with the other groups of rats. Electron microscopical analysis revealed similar findings as described after TNF-alpha alone, although the effects were more prominent at all time points after perfusion. In conclusion, our findings suggest that the enhanced anti-tumour effect after the combination of TNF-alpha with melphalan results from potentiation of the TNF-alpha-induced vascular changes accompanied by increased vascular permeability and platelet aggregation. This may result in additive cytotoxicity or inhibition of growth of residual tumour cells.
使用肿瘤坏死因子α(TNF-α)和美法仑进行的隔离肢体灌注(ILP)在患有不可切除的软组织肉瘤和肢体III期黑色素瘤的患者中显示出令人印象深刻的结果。TNF-α和美法仑在体内协同抗肿瘤作用的机制尚不完全清楚。我们在大鼠中建立了一个使用非免疫原性肉瘤的ILP模型,在该模型中观察到了类似的体内协同作用。本研究的目的是分析TNF-α与美法仑联合产生这种协同反应的形态学基础,以更深入了解其中的发病机制。对生理盐水处理组(n = 14)和美法仑处理组(n = 11)大鼠的肿瘤进行组织学检查发现,超过80%的横截面中肿瘤细胞明显存活。在肿瘤的其余部分观察到间质水肿和凝固性坏死。几乎没有出血。TNF-α处理组(n = 22)出现明显水肿、充血、血管淤血、红细胞外渗和出血性坏死(20%-60%的横截面)。水肿和出血表明微血管通透性和完整性发生了剧烈改变。通过光学显微镜和电子显微镜观察,我们发现出血先于全身性血小板聚集。因此,我们认为观察到的血小板聚集是微血管损伤的结果而非其引发因素。值得注意的是,这些事件几乎不影响肿瘤生长。然而,与其他组大鼠相比,用TNF-α和美法仑联合灌注组(n = 24)显示出更广泛的出血性坏死(80%-90%的横截面),并显示出更长的缓解期(平均11天)。电子显微镜分析揭示了与单独使用TNF-α后描述的类似结果,尽管在灌注后的所有时间点效果都更显著。总之,我们的研究结果表明,TNF-α与美法仑联合后增强的抗肿瘤作用源于TNF-α诱导的血管变化的增强,伴有血管通透性增加和血小板聚集。这可能导致附加的细胞毒性或抑制残留肿瘤细胞的生长。