title: p53 reactivation kills KSHV lymphomas efficiently in vitro and in vivo: new hope for treating aggressive viral lymphomas.
abstract: KSHV 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.
authors: Genome-Scale Biology Program, Biomedicum Helsinki, Institute of Biomedicine, University of Helsinki, Helsinki, Finland.
authors: Grzegorz
authors: G
authors: Sarek
authors: Päivi M
authors: PM
authors: Ojala
mesh_terms: D000818:Animals; D019288:Herpesvirus 8, Human / Q000254:growth & development / Q000472:pathogenicity*; D006801:Humans; D016483:Lymphoma, AIDS-Related / Q000378:metabolism / Q000473:pathology / Q000628:therapy* / Q000821:virology*; D012514:Sarcoma, Kaposi / Q000378:metabolism / Q000473:pathology / Q000628:therapy* / Q000821:virology*; D015398:Signal Transduction / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism* / Q000502:physiology
chemical_list: D016159:Tumor Suppressor Protein p53