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JNCI Journal of the National Cancer Institute 2006 98(21):1546-1557; doi:10.1093/jnci/djj413
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© 2006 The Author(s). This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

ARTICLE

Effects of Intravenously Administered Recombinant Vesicular Stomatitis Virus (VSV{Delta}M51) on Multifocal and Invasive Gliomas

XueQing Lun, Donna L. Senger, Tommy Alain, Andra Oprea, Kelley Parato, Dave Stojdl, Brian Lichty, Anthony Power, Randal N. Johnston, Mark Hamilton, Ian Parney, John C. Bell, Peter A. Forsyth

Affiliations of authors: Departments of Oncology, Clinical Neurosciences, and Biochemistry and Molecular Biology, Tom Baker Cancer Centre (XL, DLS, TA, AO, RNJ, IP, PAF), Clark H. Smith Integrative Brain Tumor Research Center (XL, DLS, TA, AO, MH, IP, PAF), Department of Neurosurgery (MH), University of Calgary, AB, Canada; Ottawa Regional Cancer Centre Research Laboratories, Ottawa, ON, Canada (KP, AP, JCB); Apoptosis Research Center, Children's Hospital of Eastern Ontario, Ottawa, ON, Canada (DS); Centre for Gene Therapeutics, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada (BL)

Correspondence to: Peter A. Forsyth, MD, Clark H. Smith Integrative Brain Tumor Research Center, Rm. 372A, Heritage Medical Research Building, 3330 Hospital Dr. NW, Calgary, AB T2N 4N1, Canada (e-mail: pforsyth{at}ucalgary.ca).

Background: An ideal virus for the treatment of cancer should have effective delivery into multiple sites within the tumor, evade immune responses, produce rapid viral replication, spread within the tumor, and infect multiple tumors. Vesicular stomatitis virus (VSV) has been shown to be an effective oncolytic virus in a variety of tumor models, and mutations in the matrix (M) protein enhance VSV's effectiveness in animal models. Methods: We evaluated the susceptibility of 14 glioma cell lines to infection and killing by mutant strain VSV{Delta}M51, which contains a single–amino acid deletion in the M protein. We also examined the activity and safety of this strain against the U87 and U118 experimental models of human malignant glioma in nude mice and analyzed the distribution of the virus in the brains of U87 tumor–bearing mice using fluorescence labeling. Finally, we examined the effect of VSV{Delta}M51 on 15 primary human gliomas cultured from surgical specimens. All statistical tests were two-sided. Results: All 14 glioma cell lines were susceptible to VSV{Delta}M51 infection and killing. Intratumoral administration of VSV{Delta}M51 produced marked regression of malignant gliomas in nude mice. When administered systemically, live VSV{Delta}M51 virus, as compared with dead virus, statistically significantly prolonged survival of mice with unilateral U87 tumors (median survival: 113 versus 46 days, P = .0001) and bilateral U87 tumors (median survival: 73 versus 46 days, P = .0025). VSV{Delta}M51 infected multifocal gliomas, invasive glioma cells that migrated beyond the main glioma, and all 15 primary human gliomas. There was no evidence of toxicity. Conclusions: Systemically delivered VSV{Delta}M51 was an effective and safe oncolytic agent against laboratory models of multifocal and invasive malignant gliomas, the most challenging clinical manifestations of this disease.


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