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Systemic Delivery of ₁34.5-Deleted Herpes Simplex Virus-1 Selectively Targets and Treats Distant Human Xenograft Tumors That Express High MEK Activity

Departments of ¹ Surgery and ² Radiation and Cellular Oncology, ³ Center for Molecular Oncology, ⁴ Ludwig Center for Metastasis Research, and ⁵ The Marjorie B. Kovler Viral Oncology Laboratories, University of Chicago, Chicago, Illinois

Requests for reprints: Ralph R. Weichselbaum, Department of Radiation and Cellular Oncology, Center for Advanced Medicine 1338 (MC 9006), 5758 South Maryland Avenue, Chicago, IL 60637. Phone: 773-702-0817; Fax: 773-834-7233; E-mail: rrw{at}radonc.uchicago.edu.

₁34.5 mutant herpes simplex type 1 viruses are under active clinical investigation as oncolytic therapy for cancer. Mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK) activity has been shown to suppress protein kinase R and thereby confer oncolytic susceptibility to some human tumors by R3616, a virus deleted for both copies of ₁34.5. We report that systemic delivery of R3616 can selectively target and destroy human xenograft tumors that overexpress MEK activity compared with tumors that express lower MEK activity. These results suggest systemic delivery of R3616 may be effective in the treatment of some human tumors. [Cancer Res 2007;67(17):8301–6]