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p53 reactivation kills KSHV lymphomas efficiently in vitro and in vivo: new hope for treating aggressive viral lymphomas Sarek G; Ojala PMCell Cycle 2007[Sep]; 6 (18): 2205-9KSHV infection is the causative agent in three different tumor types: Kaposi's sarcoma, a plasmablastic variant of multicentric Castelman's disease and an AIDS-related form of B cell lymphoproliferative disorder called primary effusion lymphoma (PEL). PEL manifests as an effusion malignancy in Kaposi's sarcoma patients with advanced AIDS, but also occurs in HIV-negative individuals. PEL is a very aggressive disease, and currently there are no efficient therapies for treating PEL. In our recent paper we report that p53 reactivation by a small molecule inhibitor of p53-MDM2 interaction, Nutlin-3a, induces selective and massive apoptosis in PEL cells, and has striking anti-tumor activity in a mouse xenograft PEL model. In the light of current treatment regimens for PEL, we discuss here the benefits of using reactivation of the p53 pathway as a novel principle for the treatment of this virally induced highly aggressive malignancy.|Animals[MESH]|Herpesvirus 8, Human/growth & development/*pathogenicity[MESH]|Humans[MESH]|Lymphoma, AIDS-Related/metabolism/pathology/*therapy/*virology[MESH]|Sarcoma, Kaposi/metabolism/pathology/*therapy/*virology[MESH]|Signal Transduction/physiology[MESH]|Tumor Suppressor Protein p53/*metabolism/physiology[MESH] |
