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p53 Reactivation Kills KSHV Lymphomas Efficiently In Vitro and In Vivo: New Hope for Treating Aggressive Viral Lymphomas

Grzegorz Sarek and Päivi M. Ojala

volume 6 | issue 18

15 September 2007
Pages: 2205 - 2209

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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 human immunodeficiency virus-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 1. 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

Grzegorz Sarek

University of Helsinki; Helsinki, Finland

Päivi M. Ojala

University of Helsinki; Helsinki, Finland


Purchase article for $19

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