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Immunological Prevention of a Multigene Cancer Syndrome

¹ Cancer Research Section, Department of Experimental Pathology and ³ Interdepartment Center for Cancer Research "Giorgio Prodi," University of Bologna, Bologna, Italy; ² Istituti Ortopedici Rizzoli, Bologna, Italy; ⁴ Center of Excellence on Aging (CeSI), "G. D’Annunzio" University, Chieti, Italy; and ⁵ Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy

Vaccines effectively prevent the onset of tumors in transgenic mice carrying activated oncogenes; however, human tumors are caused by combined alterations in oncogenes and oncosuppressor genes. We evaluated the impact of prophylactic vaccines in HER-2/neu transgenic, p53 wild-type/null mice that succumb to an aggressive cancer syndrome comprising mammary and salivary gland carcinomas and rhabdomyosarcoma. A vaccine made of allogeneic mammary carcinoma cells expressing HER-2/neu and interleukin 12 afforded long-term protection from tumor onset. Tumor prevention was mediated by T cell–derived cytokines, in particular -interferon, and by anti–HER-2/neu antibodies. HER-2/neu expression was inhibited in target tissues of vaccinated mice, and somatic loss of the wild-type p53 allele did not occur. A highly effective vaccine against a single oncoprotein induced a powerful immune response that arrested multistep carcinogenesis in distinct target tissues.

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				T. Pannellini, M. Spadaro, E. Di Carlo, E. Ambrosino, M. Iezzi, A. Amici, P. L. Lollini, G. Forni, F. Cavallo, and P. Musiani Timely DNA Vaccine Combined with Systemic IL-12 Prevents Parotid Carcinomas before a Dominant-Negative p53 Makes Their Growth Independent of HER-2/neu Expression. J. Immunol., June 15, 2006; 176(12): 7695 - 7703. [Abstract] [Full Text] [PDF]