. Author manuscript; available in PMC: 2009 Aug 1.

Published in final edited form as: Mol Ther. 2008 Jun 10;16(8):1382–1391. doi: 10.1038/mt.2008.112

Table 1. Oncolytic hrR3-induced changes in angiogenic and angiostatic factors in rat glioma 12 hours after oncolytic virus (OV) infection.

Gene name	untreated (fold/actin)	OV treated (fold/actin)	Fold Induced	P value	Implicated in HSV-1 pathology	Implicated in glioma angiogenesis
VEGF	0.018	0.012	0.667	0.298	Yes²⁷	Yes³³
MMP9	0.001	0.004	4.000	0.0194	Yes⁴³	Yes³²
TSP-1	0.130	0.069	0.531	0.0050	Yes⁴⁴	Yes²⁵
CYR61^a	0.031	0.277	8.940	0.0012	ND	Yes⁴⁵
bFGF	0.00085	0.00125	1.470	0.39	ND	Yes⁴⁶
PDGF	0.779	0.476	0.611	0.122	ND	Yes³⁶
MMP2	0.0061	0.00033	0.054	0.0057	ND	Yes
Ang1	0.004	0.003	0.750	0.218	ND	Yes³⁷
Ang-2^a	0.0026	0.0096	3.730	0.0028	ND	Yes⁴⁷
SF/HGF	0.0001	0.00007	0.700	0.586	ND	Yes⁴⁸,⁴⁹
BAI1	0.00248	0.00245	0.988	0.9630	ND	Yes²⁰

Abbreviations: bFGF, basic fibroblast growth factor; HSV-1, herpes simplex virus 1; MMP9, matrix metalloproteinase 9; ND, not determined; PDGF, platelet derived growth factor; VEGF, vascular endothelial growth factor.

Changes in the angiogenic profile of tumors derived from rats with D74/HveC glioma cells 12 hours after treatment with oncolytic HSV-1 (hrR3). The animals were killed after 12 hours, total RNA was obtained from each tumor tissue, and the levels of indicated gene expression relative to endogenous β-actin were evaluated by quantitative real-time PCR, as described.

Genes which are significantly induced upon OV infection of tumors. Genes with a significant change in expression upon OV infection are in bold.