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The Rgr Oncogene Induces Tumorigenesis in Transgenic Mice

¹ Department of Pathology and New York University Cancer Institute, New York University School of Medicine, New York, New York; ² Molecular Pathology and Molecular Oncology Program, Centro Nacional de Investigaciones Oncológicas, Madrid, Spain; and ³ Center for Experimental Research and Medical Studies, University of Turin, Turin, Italy

To study the oncogenic potential of Rgr in vivo, we have generated several transgenic Rgr mouse lines, which express the oncogene under the control of different promoters. These studies revealed that Rgr expression leads to the generation of various pathological alterations, including fibrosarcomas, when its transgenic expression is restricted to nonlymphoid tissues. Moreover, the overall incidence and latency of fibrosarcomas were substantially increased and shortened, respectively, in a p15^INK4b-defective background. More importantly, we also have demonstrated that Rgr expression in thymocytes of transgenic mice induces severe alterations in the development of the thymocytes, which eventually lead to a high incidence of thymic lymphomas. This study demonstrates that oncogenic Rgr can induce expression of p15^INK4b and, more importantly, that both Rgr and p15^INK4b cooperate in the malignant phenotype in vivo. These findings provide new insights into the tumorigenic role of Rgr as a potent oncogene and show that p15^INK4b can act as a tumor suppressor gene.

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