Bortezomib-induced Epstein–Barr virus and Kaposi sarcoma herpesvirus lytic gene expression: oncolytic strategiesReid, Erin G.Current Opinion in Oncology: September 2011 - Volume 23 - Issue 5 - p 482–487 doi: 10.1097/CCO.0b013e3283499c37 Cancer in AIDS: Edited by Ronald Mitsuyasu Abstract Author Information Purpose of review Gamma herpesviruses (GHVs) are responsible for a substantial proportion of virus-associated human cancers, particularly in immunocompromised individuals. Methods that employ lytic activation of viruses latently infecting tumors represent a novel strategy of antineoplastic therapy. Recent findings The proteasome inhibitor, bortezomib, has been shown to be a potent activator of GHV lytic cycle and has demonstrated activity in case reports of GHV-related malignancies. Although initial reports implicated the inhibition of the NF-κB pathway, more recent studies identify alternative pathways responsible for bortezomib-mediated lytic induction of GHVs and activity against the malignancies that harbor them. Summary Further exploration of proteasome inhibition as an oncolytic strategy is warranted and will require clinical/translational trials to determine whether lytic induction of GHVs correlates with clinical response to bortezomib, and, if so, to optimize this oncolytic strategy. Moores UCSD Cancer Center, La Jolla, California, USA Correspondence to Erin G. Reid, MD, MS, Associate Professor of Medicine, Moores UCSD Cancer Center, 3855 Health Sciences Drive, La Jolla, CA 92093-0987, USA Tel: +1 858 822 6276; fax: +1 858 822 6288; e-mail: email@example.com © 2011 Lippincott Williams & Wilkins, Inc.