The tmnom-associated antigen mucin 1 (MUCI) is a mnltifimctional protein involved in protection of muckous membranes, signal transduction, and mOdulation of the immume system. More than 70% of cancers overexpress MUCI, making MUC 1 a potential target for immnnotber apy. In the present study, MUCI transgenic mice were crossed with syngeneic strains that express the polyomavirus middle-T oncogene (PyMT) diiven by the mouse mammary tumour virus promoter long teminal repeat (MMTV-LTR). The resultant breed (MMT mice) developed spontaneous MUCI expressing mammary cmcinomas with 100% penetrance at 8-15 weeks of age. As fOund in buman breast cancer, the mammary carcinoma in MMT mice arose in multiple stages, Immumization with fusions of dendritic cells and MUC 1-positive tumour cells (PC/MUC1) induced MUCI specific immune responses that blocked or delayed the development of sponta neons breast carcinomas, in contrast, there was no delay of tumour development in MMT mice immmunized with in-adiated MC38/MUCI tumonr cells. The efficacy of fusion cells was closely correlated with the timing of initial immmlization, immumization with FC/MUCI initiated in MMT mice at<1, 1-2 and 2-3 months of age rendered 33, 5 and 0% of mice free of remora, respectively, up to 6 months. Whereas mice immunized in the later stage of tumour development succumbed to their disease, immunization resulted in control of tumour progression and prolongation of life. These results indicate that immunization with FC/MUC1 can generate an anti-MUCI response that is sufficient to delay the development of spontaneous mammary carcinomas and control tumour progression in MMT mice.