Watanabe N, Niitsu Y, Umeno H, Kuriyama H, Neda H, Yamauchi N, Maeda M, Urushizaki I
Department of Internal Medicine, Sapporo Medical College, Japan.
Cancer Res. 1988 Apr 15;48(8):2179-83.
Stereoscopic observation via an implanted sight glass in mice bearing transplanted methylcholanthrene-induced A-cells showed tumorivascular hemorrhage at 1-2 h after tumor necrosis factor (TNF) administration, congestion at 4-6 h, and hemorrhage, congestion, and blood circulation blockage at 24 h. Histological examination after TNF administration to mice bearing similar methylcholanthrene-induced A-cell transplants showed thrombus formation in the tumor vasculature at 4 h and thereafter. Suppression of this thrombus formation with heparin had no apparent influence on the necrotic response, tumor growth inhibition or complete cure rate following TNF administration to mice bearing the methylcholanthrene-induced A-cell tumors. The results suggest that direct toxicity of TNF on tumor vasculature is a factor in the overall antitumor mechanism of TNF.
通过植入视镜对携带甲基胆蒽诱导的A细胞移植瘤的小鼠进行立体观察，结果显示，给予肿瘤坏死因子（TNF）后1 - 2小时肿瘤血管出现出血，4 - 6小时出现充血，24小时出现出血、充血和血液循环阻断。对携带类似甲基胆蒽诱导的A细胞移植瘤的小鼠给予TNF后进行组织学检查，结果显示4小时及之后肿瘤血管中形成血栓。用肝素抑制这种血栓形成，对给予TNF的携带甲基胆蒽诱导的A细胞肿瘤的小鼠的坏死反应、肿瘤生长抑制或完全治愈率没有明显影响。结果表明，TNF对肿瘤血管的直接毒性是TNF整体抗肿瘤机制中的一个因素。
