研究了MUC1特异性DNA免疫对MUC1转基因人类小鼠（MUC1.Tg）炎症驱动的结肠癌发生的预防效果。小鼠接种了MUC1 DNA混合自体骨髓来源的树突状细胞（BMDCs），然后通过苯并氧嘧啶（AOM）注射和口服硫酸葡萄糖酸钠（DSS）诱发结肠肿瘤。观察到两种类型的肿瘤，即鳞状上皮化生和管状腺瘤。两者都表达了高水平的MUC1，因为不同特异性的抗-MUC1抗体结合，而正常结肠粘膜中未检测到MUC1表达。当小鼠接种MUC1 DNA + BMDCs时，肿瘤发生率，肿瘤数量和肿瘤大小显着降低。相反，单独接种MUC1 DNA或BMDCs无法减少肿瘤负担。由DSS引起的炎症未被MUC1 DNA + BMDCs疫苗抑制。此外，在接种后生长的肿瘤中，由抗-MUC1抗体结合判断的MUC1蛋白表达水平与对照组没有显著差异。总之，在MUC1.Tg小鼠中建立了一个炎症驱动的癌症模型，与人类结肠癌发生密切相关。在这个模型中，通过一种不影响结肠炎症水平的机制，MUC1 DNA + BMDCs疫苗接种对MUC1耐受性具有覆盖作用并减少肿瘤负担是有效的。

The preventive efficacy of MUC1-specific DNA immunization on inflammation-driven colon carcinogenesis in human MUC1 transgenic (MUC1.Tg) mice was investigated. Mice were vaccinated with MUC1 DNA mixed with autologous bone-marrow-derived dendritic cells (BMDCs), and then colonic tumors were induced by azoxymethane (AOM) injection and oral administration of dextran sulfate sodium (DSS). Two types of tumors, squamous metaplasia and tubular adenoma, were observed. Both expressed high levels of MUC1 as indicated by the binding of anti-MUC1 antibodies with different specificities, whereas MUC1 expression was not detected in normal colonic mucosa. When mice were immunized with MUC1 DNA + BMDCs, tumor incidence, tumor number, and tumor size were significantly reduced. In contrast, vaccination with MUC1 DNA alone or BMDCs alone was ineffective in reducing tumor burden. Inflammation caused by DSS was not suppressed by the MUC1 DNA + BMDCs vaccination. Furthermore, MUC1 protein expression levels, as judged by anti-MUC1 antibody binding in tumors grown after vaccination, did not significantly differ from the control. In conclusion, an inflammation-driven carcinogenesis model was established in MUC1.Tg mice, closely resembling human colon carcinogenesis. In this model, vaccination with MUC1 DNA + BMDCs was effective in overriding MUC1 tolerance and reducing the tumor burden by a mechanism not affecting the level of colonic inflammation.