Sanada E, Fuchimoto S, Orita K
First Department of Surgery, Okayama University Medical School, Japan.
Acta Med Okayama. 1990 Aug;44(4):217-22. doi: 10.18926/AMO/30421.
To prevent the development of hepatic metastases after surgery for colorectal cancer, it is important to inhibit the growth of any micrometastases which occur during the operation. We used a hepatic metastasis model in mice to investigate the effects of combination therapy with natural human tumor necrosis factor-alpha (nHuTNF-alpha) and natural murine interferon-alpha/beta (nMuIFN-alpha/beta). Decreased formation of hepatic metastases by murine colon-26 carcinoma was recognized following a single injection of nHuTNF-alpha, nMuIFN-alpha/beta, or both. These inhibitory effects were synergistic. NK activity was also measured, because notaral lerller cells not only have an anti-tumor effect but are also a representative of the host immune system. Both nHuTNF-alpha and nMuIFN-alpha/beta were able to activate NK cells, and the combination of the cytokines more significantly augmented NK activity. The in vivo elevation of NK activity induced by nHuTNF-alpha, nMuIFN-alpha/beta, or their combination may be one of the mechanisms of their antiproliferative effect on experimental hepatic metastases of murine colon-26 carcinoma.
为预防结直肠癌手术后肝转移的发生，抑制手术过程中出现的任何微转移灶的生长至关重要。我们使用小鼠肝转移模型来研究天然人肿瘤坏死因子-α（nHuTNF-α）与天然鼠干扰素-α/β（nMuIFN-α/β）联合治疗的效果。单次注射nHuTNF-α、nMuIFN-α/β或两者后，可观察到小鼠结肠-26癌肝转移灶形成减少。这些抑制作用具有协同性。还检测了自然杀伤（NK）活性，因为自然杀伤细胞不仅具有抗肿瘤作用，也是宿主免疫系统的代表。nHuTNF-α和nMuIFN-α/β均能激活NK细胞，且细胞因子联合使用能更显著地增强NK活性。nHuTNF-α、nMuIFN-α/β或其联合使用诱导的体内NK活性升高可能是其对小鼠结肠-26癌实验性肝转移具有抗增殖作用的机制之一。
