Treatment of experimental subcutaneous human melanoma with a replication-restricted herpes simplex virus mutant
BP Randazzo, MG Bhat, S Kesari, NW Fraser… - Journal of investigative …, 1997 - Elsevier
BP Randazzo, MG Bhat, S Kesari, NW Fraser, SM Brown
Journal of investigative dermatology, 1997•ElsevierModified, non-neurovirulent herpes simplex viruses (HSV) have shown promise for the
treatment of brain tumors, including intracranial melanoma. In this report, we show that HSV-
1716, an HSV-1 mutant lacking both copies of the gene coding-infected cell protein 34.5
(ICP 34.5), can effectively treat experimental subcutaneous human melanoma in mice. In
vitro, HSV-1716 replicated in all 26 human melanoma cell lines tested, efficiently lysing the
cells. Therapeutic infection of subcutaneous human melanoma nodules with HSV-. 171.6 …
treatment of brain tumors, including intracranial melanoma. In this report, we show that HSV-
1716, an HSV-1 mutant lacking both copies of the gene coding-infected cell protein 34.5
(ICP 34.5), can effectively treat experimental subcutaneous human melanoma in mice. In
vitro, HSV-1716 replicated in all 26 human melanoma cell lines tested, efficiently lysing the
cells. Therapeutic infection of subcutaneous human melanoma nodules with HSV-. 171.6 …
Modified, non-neurovirulent herpes simplex viruses (HSV) have shown promise for the treatment of brain tumors, including intracranial melanoma. In this report, we show that HSV-1716, an HSV-1 mutant lacking both copies of the gene coding-infected cell protein 34.5 (ICP 34.5), can effectively treat experimental subcutaneous human melanoma in mice. In vitro, HSV-1716 replicated in all 26 human melanoma cell lines tested, efficiently lysing the cells. Therapeutic infection of subcutaneous human melanoma nodules with HSV-.171.6 led to viral replication that was restricted to tumor cells by immunohistochemistry. Moreover, HSV-1716 treatment significantly inhibited progression of preformed subcutaneous human melanoma nodules in SCID mice and caused complete regression of some tumors. This work expands the potential scope of HSV-1-based cancer therapy.
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