It has been shown previously that A60, an antigen complex ofMycobacterium hovisBCG, triggers humoral and cellular immune reactionsin vivoand lymphocyte‐dependent macrophage activationin vitro.In the present work, the ability of A60 to prevent murine tumour development, in conjunction or not with irradiated isologous cancer cells, was explored with Taper liver tumour (TLT), a mammar‐y‐derived neoplasm (EMT6), and Lewis lung carcinoma (3LL). Repeated injections of A60 prior to challenge reduced the incidence of EMT6 and 3LL solid tumours and increased life span. This effect was enhanced by simultaneous administration of 7‐irradiated cancer cells (80–100% suppression of EMT6 and 3LL tumour growth). In mice developing or rejecting tumours, the status of humoral and cellular immunity was evaluated by A60‐based immunoassays. Tumor development was accompanied by a rapid decrease of both anti‐A60 IgG titre in blood and A60‐triggered delayed hypersensitivity reactions. Moreover, A60‐induced T lymphocyte proliferation and macrophage‐dependent autologous cancer cell cytolysis declined progressively during the course of tumour growth. In case of successful immuno‐therapy, a pattern similar to that of unchallenged controls was observed. Our results suggest that A60 promotes cancer rejection via tumour infiltration by lymphocytes and macrophages activated by A60‐specific T lymphocytes. An increased processing of tumour‐specific antigens and activation of tumour‐infiltrating lymphocytes is induced by administration of irradiated cancer ce