Kanazawa J, Ohta S, Shitara K, Fujita F, Fujita M, Hanai N, Akinaga S, Okabe M
Pharmaceutical Research Institute, Kyowa Hakko Kogyo Co Ltd, Sunto-gun, Shizuoka-ken, Japan.
Cancer Immunol Immunother. 2000 Jul;49(4-5):253-8. doi: 10.1007/s002620000101.
KM871 is a chimeric antibody recognizing ganglioside GD3, which is one of the major gangliosides expressed on the cell surface of human tumors of neuroectodermal origin. This study demonstrates the antitumor activity of KM871 against human melanoma xenografts in nude mice, and analyzes the effector function operating in mice. In a well-established tumor model, KM871 showed antitumor activity against H-15 and SK-MEL-28 human melanoma but not against H-187 and G361 human melanoma when administered intravenously 5 days/week for 2 weeks. The G361 tumor became sensitive when KM871 was first administered on the day of tumor inoculation. In this assay, it was observed that almost all the mice were tumor-free, but a few mice developed tumors. Therefore, we examined the amount and expression pattern of GD3 antigen on G361 tumors escaping from KM871 treatment, but no change was observed. Next we examined the optimal administration schedule for KM871 in mice, using H-15 melanoma. KM871 showed antitumor activity when administered intravenously either 5 days/week for 2 weeks or three biweekly doses. However, the effect of the former schedule was stronger than three biweekly doses. To compare the effector function in humans and mice, we studied the complement-mediated cytotoxicity, antibody-dependent cell-mediated cytotoxicity and antibody-dependent macrophage-mediated cytotoxicity of KM871 using complement or effector cells prepared from humans and mice. It was found that the antibody-dependent cell-mediated cytotoxicity exerted by polymorphonuclear cells and antibody-dependent macrophage-mediated cytotoxicity were the only antitumor mechanism of KM871 in mice. However their action was very weak compared with that in humans, and complement-mediated cytotoxicity, which was strong in humans, was not observed in mice. Therefore, the antitumor activity of KM871 against human melanomas evaluated by the nude mouse model might be underestimated. These results indicate that KM871 shows good antitumor activity against GD3-positive human melanoma and the antitumor activity expected in humans might be superior to that of the nude mouse model.
KM871是一种识别神经节苷脂GD3的嵌合抗体,GD3是在神经外胚层起源的人类肿瘤细胞表面表达的主要神经节苷脂之一。本研究证明了KM871对裸鼠人黑色素瘤异种移植瘤的抗肿瘤活性,并分析了在小鼠体内发挥作用的效应功能。在一个成熟的肿瘤模型中,当每周静脉注射5天,持续2周时,KM871对H-15和SK-MEL-28人黑色素瘤显示出抗肿瘤活性,但对H-187和G361人黑色素瘤没有活性。当在肿瘤接种当天首次给予KM871时,G361肿瘤变得敏感。在该试验中,观察到几乎所有小鼠都没有肿瘤,但有几只小鼠出现了肿瘤。因此,我们检查了从KM871治疗中逃逸的G361肿瘤上GD3抗原的数量和表达模式,但未观察到变化。接下来,我们使用H-15黑色素瘤研究了KM871在小鼠中的最佳给药方案。当每周静脉注射5天,持续2周或每两周注射三次时,KM871显示出抗肿瘤活性。然而,前一种给药方案的效果比每两周注射三次更强。为了比较人和小鼠中的效应功能,我们使用从人和小鼠制备的补体或效应细胞研究了KM871的补体介导的细胞毒性、抗体依赖性细胞介导的细胞毒性和抗体依赖性巨噬细胞介导的细胞毒性。发现多形核细胞发挥的抗体依赖性细胞介导的细胞毒性和抗体依赖性巨噬细胞介导的细胞毒性是KM871在小鼠中的唯一抗肿瘤机制。然而,与在人类中的作用相比,它们的作用非常微弱,并且在小鼠中未观察到在人类中很强的补体介导的细胞毒性。因此,通过裸鼠模型评估的KM871对人类黑色素瘤的抗肿瘤活性可能被低估。这些结果表明,KM871对GD3阳性人类黑色素瘤显示出良好的抗肿瘤活性,并且在人类中预期的抗肿瘤活性可能优于裸鼠模型。