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Robert H. Silverman, PhD

Professor, Cancer Biology 216.445.9650 (o) 216.445.6269 (f)

Member, GU Malignancies Program


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Our studies probe fundamental molecular and cellular processes that impact microbial infections and cancer. We seek a better understanding of how the mammalian cell resists viral infections and how the virus antagonizes the host response to infection. Interferons (IFNs) induce a family of 2',5'-oligoadenylate (2-5A) synthetases (OAS). In response to viral double-stranded RNA, OAS produces 2-5A whose function is to activate RNase L causing degradation of viral and cellular RNA. Previously we cloned RNase L and established its antiviral activities in genetically deficient mice. We found that RNase L cleaves viral and cellular RNA to generate small RNAs that stimulate IFN synthesis through RIG-I and MDA5. We are currently studying viral and host 2',5'-phosphodiesterases that prevent activation of RNase L, thus allowing virus replication and viral pathogenesis.  Our goals include elucidating fundamental events and biologic endpoints surrounding RNase L that impact on viral replication cycles and tumor biology. Another area of research concerns the roles of innate immunity and genetics in prostate cancer. The hereditary prostate cancer 1 (HPC1) gene maps to RNase L. We are investigating the potential role of RNase L in prostate cancer by focusing on basic cellular processes regulated by RNase L including autophagy and apoptosis. We are also developing an experimental protocol for treating late-stage cancer by combining sunitinib treatments with infection by an oncolytic virus.

interferon; rnase l; antiviral innate immunity; prostate cancer; oncolytic virotherapy