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Development of Rhabdomyosarcoma in HER-2/neu Transgenic p53 Mutant Mice¹

Cancer Research Section, Department of Experimental Pathology, University of Bologna, I-40126 Bologna [P. N., G. N., C. D. G., S. C., A. A., L. L., P-L. L.]; Istituti Ortopedici Rizzoli, I-40136 Bologna [G. N., L. L.]; and Department of Oncology and Neurosciences, G. D’Annunzio University, I-66013 Chieti [E. D. C., M. I., P. M.], Italy

Rhabdomyosarcomas derive from the skeletal muscle lineage and harbor a variety of genetic and molecular lesions. However, it is not clear which molecular alterations have a pathogenetic role. We show that activation of the HER-2/neu oncogene coupled with inactivation of the oncosuppressor gene p53 causes rhabdomyosarcoma in mice. At the age of 11–21 weeks, all male mice carrying both genetic lesions developed embryonal rhabdomyosarcomas expressing desmin, myosin, and insulin-like growth factor-II, in the genitourinary tract. Our findings led to the hypothesis that the interaction between HER family genes and the p53 pathway might be involved in the origin of human rhabdomyosarcoma.

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