Erin G Reid1. 1. Moores UCSD Cancer Center, La Jolla, California 92093-0987, USA. egreid@ucsd.edu
Abstract
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.
PURPOSE OF REVIEW: Gamma herpesviruses (GHVs) are responsible for a substantial proportion of virus-associated humancancers, 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.
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