p53 reactivation kills KSHV lymphomas efficiently in vitro and in vivo: new hope for treating aggressive viral lymphomas

Cell Cycle. 2007 Sep 15;6(18):2205-9. doi: 10.4161/cc.6.18.4730. Epub 2007 Jul 10.


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.

Publication types

  • Review

MeSH terms

  • Animals
  • Herpesvirus 8, Human / growth & development
  • Herpesvirus 8, Human / pathogenicity*
  • Humans
  • Lymphoma, AIDS-Related / metabolism
  • Lymphoma, AIDS-Related / pathology
  • Lymphoma, AIDS-Related / therapy*
  • Lymphoma, AIDS-Related / virology*
  • Sarcoma, Kaposi / metabolism
  • Sarcoma, Kaposi / pathology
  • Sarcoma, Kaposi / therapy*
  • Sarcoma, Kaposi / virology*
  • Signal Transduction / physiology
  • Tumor Suppressor Protein p53 / metabolism*
  • Tumor Suppressor Protein p53 / physiology


  • Tumor Suppressor Protein p53