QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:
Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (11) Citing Articles via Google Scholar Google Scholar Articles by Merrill, M. K. Articles by Gromeier, M. Search for Related Content PubMed PubMed Citation

Poliovirus receptor CD155-targeted oncolysis of glioma

Departments of Molecular Genetics and Microbiology (M.K.M., M.G.), Surgery (J.H.S.), and Pathology (C.J.W., D.D.B.), Duke University Medical Center, Durham, NC 27710, USA; and Institute of Immunology, Hanover Medical University, 30625 Hanover, Germany (G.B.)

² Address correspondence to Matthias Gromeier, Department of Molecular Genetics and Microbiology, Duke University Medical Center, Box 3020, Durham, NC 27710 (grome001{at}mc.duke.edu).

Abstract

Cell adhesion molecules of the immunoglobulin superfamily are aberrantly expressed in malignant glioma. Amongst these, the human poliovirus receptor CD155 provides a molecular target for therapeutic intervention with oncolytic poliovirus recombinants. Poliovirus has been genetically modified through insertion of regulatory sequences derived from human rhinovirus type 2 to selectively replicate within and destroy cancerous cells. Efficacious oncolysis mediated by poliovirus derivatives depends on the presence of CD155 in targeted tumors. To prepare oncolytic polioviruses for clinical application, we have developed a series of assays in high-grade malignant glioma (HGL) to characterize CD155 expression levels and susceptibility to oncolytic poliovirus recombinants. Analysis of 6 HGL cases indicates that CD155 is expressed in these tumors and in primary cell lines derived from these tumors. Upregulation of the molecular target CD155 rendered explant cultures of all studied tumors highly susceptible to a prototype oncolytic poliovirus recombinant. Our observations support the clinical application of such agents against HGL.

This article has been cited by other articles:

				S. A. Campbell, M. Mulvey, I. Mohr, and M. Gromeier Attenuation of Herpes Simplex Virus Neurovirulence with Picornavirus cis-Acting Genetic Elements J. Virol., January 15, 2007; 81(2): 791 - 799. [Abstract] [Full Text] [PDF]

				M. K. Merrill, E. Y. Dobrikova, and M. Gromeier Cell-Type-Specific Repression of Internal Ribosome Entry Site Activity by Double-Stranded RNA-Binding Protein 76. J. Virol., April 1, 2006; 80(7): 3147 - 3156. [Abstract] [Full Text] [PDF]

				H. Ochiai, S. A. Campbell, G. E. Archer, T. A. Chewning, E. Dragunsky, A. Ivanov, M. Gromeier, and J. H. Sampson Targeted Therapy for Glioblastoma Multiforme Neoplastic Meningitis with Intrathecal Delivery of an Oncolytic Recombinant Poliovirus Clin. Cancer Res., February 15, 2006; 12(4): 1349 - 1354. [Abstract] [Full Text] [PDF]

				K. E. Sloan, J. K. Stewart, A. F. Treloar, R. T. Matthews, and D. G. Jay CD155/PVR Enhances Glioma Cell Dispersal by Regulating Adhesion Signaling and Focal Adhesion Dynamics Cancer Res., December 1, 2005; 65(23): 10930 - 10937. [Abstract] [Full Text] [PDF]