Morahan P S, Schuller G B, Snodgrass M J, Kaplan A M
J Infect Dis. 1976 Jun;133 Suppl:A249-55. doi: 10.1093/infdis/133.supplement_2.a249.
Growth of tumors was inhibited or enhanced in mice by a synthetic (pyran) or a biologic (corynebacterium parvum) immunopotentiator. Marked inhibition of leukemogenesis induced by Friend leukemia virus was produced by prophylactic intraperitoneal treatment with pyran, while intravenous treatment with pyran (in the same dose and regimen) significantly enhanced growth of tumor virus. Paradoxical effects were also seen with the biologic immunopotentiator C. parvum in solid tumor systems. Treatment with C. parvum either potentiated disease or had no effect on the life span of most mice bearing the Lewis lung carcinoma. In contrast, the same treatment could produce a high percentage of tumor regressions in mice bearing the MCA 2182 sarcoma, although the effect was somewhat variable. These data, which show that a change in route of drug administration or in the type of tumor treated may reverse the effect of treatment, emphasize that the mechanism of action of immunopotentiators must be elucidated before consistent beneficial treatment of tumor viruses or tumors can be achieved.
一种合成免疫增强剂(吡喃)或一种生物免疫增强剂(短小棒状杆菌)可抑制或促进小鼠肿瘤的生长。通过吡喃预防性腹腔注射可显著抑制由Friend白血病病毒诱导的白血病发生,而用吡喃静脉注射(相同剂量和方案)则显著促进肿瘤病毒的生长。在实体瘤系统中,生物免疫增强剂短小棒状杆菌也出现了矛盾的效应。用短小棒状杆菌治疗要么增强疾病,要么对大多数携带Lewis肺癌的小鼠寿命没有影响。相比之下,相同的治疗方法可使携带MCA 2182肉瘤的小鼠产生较高比例的肿瘤消退,尽管效果有所不同。这些数据表明,给药途径的改变或所治疗肿瘤类型的改变可能会逆转治疗效果,强调在实现对肿瘤病毒或肿瘤的持续有效治疗之前,必须阐明免疫增强剂的作用机制。