Journal
MOLECULAR THERAPY
Volume 2, Issue 4, Pages 324-329Publisher
ACADEMIC PRESS INC
DOI: 10.1006/mthe.2000.0130
Keywords
herpes simplex virus; GM-CSF; melanoma; cancer therapy; Harding-Passey
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Funding
- NCI NIH HHS [CA60176] Funding Source: Medline
- NINDS NIH HHS [NS32677] Funding Source: Medline
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To evaluate the potential of defective herpes simplex virus (HSV) amplicon vectors as in vivo cytokine gene transfer vehicles for active immunotherapy, we generated a defective HSV vector that encodes the murine granulocyte-macrophage colony-stimulating factor (GM-CSF) gene, using a replication-defective HSV as helper virus. A variety of murine tumor cell lines were efficiently infected in vitro with the defective GM-CSF vector (dvGM), and this led to the synthesis and secretion of murine CM-CSF. In an established bilateral subcutaneous tumor model with Harding-Passey murine melanoma, unilateral intratumoral inoculation of dvGM significantly inhibited tumor growth of both the inoculated and noninoculated contralateral tumors. This tumor inhibition was dose-dependent and resulted in increased survival of the dvGM-treated mice. Inoculation of a lacZ-expressing defective vector had no effect: on tumor growth. We conclude that this defective HSV vector system offers an effective method for cytokine gene delivery in vivo and that GM-CSF expression in tumors has antitumor activity.
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