Kreider J W, Bartlett G L, Purnell D M
J Natl Cancer Inst. 1976 Apr;56(4):803-10. doi: 10.1093/jnci/56.4.803.
We evaluated the potential of the B16 melanoma of mice as a model system for BCG immunotherapy of malignant melanoma. We studied a variety of treatment protocols: a) BCG given simultaneously but separately with a small number of B16 cells significantly inhibited tumor growth in only three of eight experiments. b) BCG injected directly into the tumor stimulated tumor growth in three of three experiments; the stimulation was at least partially attributable to the nutrient medium in which the BCG was suspended. c) The B16 tumor was weakly immunogenic and the addition of BCG to a tumor cell vaccine offered little improvement in subsequent resistance to tumor cell challenge: d) In a model of postsurgical residual tumor, metastatic to regional lymph nodes, BCG and tumor cell vaccination did not alter the development of nodal metastases. The B16 melanoma was not a useful model system for BCG immunotherapy, because the tumor inhibition was feeble, inconsistent, and not associated with augmented tumor immunity.
我们评估了小鼠B16黑色素瘤作为恶性黑色素瘤卡介苗免疫疗法模型系统的潜力。我们研究了多种治疗方案:a) 卡介苗与少量B16细胞同时但分开给药,在八个实验中只有三个实验显著抑制了肿瘤生长。b) 将卡介苗直接注射到肿瘤中,在三个实验中有三个实验刺激了肿瘤生长;这种刺激至少部分归因于悬浮卡介苗的营养培养基。c) B16肿瘤免疫原性较弱,在肿瘤细胞疫苗中添加卡介苗对随后抵抗肿瘤细胞攻击的能力几乎没有改善:d) 在一个术后残留肿瘤转移至区域淋巴结的模型中,卡介苗和肿瘤细胞疫苗接种并未改变淋巴结转移的发展。B16黑色素瘤不是卡介苗免疫疗法的有用模型系统,因为肿瘤抑制作用微弱、不一致,且与增强的肿瘤免疫力无关。