ArticleCancer gene therapy2006
Enhancement of antitumor activity of herpes simplex virus gamma(1)34.5-deficient mutant for oral squamous cell carcinoma cells by hexamethylene bisacetamide.
Article in Cancer gene therapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Efficient Delivery and Replication of Oncolytic Virus for Successful Treatment of Head and Neck Cancer.International journal of molecular sciences · 2020Review
- Oncolytic activity of HF10 in head and neck squamous cell carcinomas.Cancer gene therapy · 2020Article
- Uncovering BRD4 hyperphosphorylation associated with cellular transformation in NUT midline carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Presage of oncolytic virotherapy for oral cancer with herpes simplex virus.The Japanese dental science review · 2017Review
- Oncolytic herpes viruses, chemotherapeutics, and other cancer drugs.Oncolytic virotherapy · 2013Review
- Entry of herpes simplex virus type 1 (HSV-1) into the distal axons of trigeminal neurons favors the onset of nonproductive, silent infection.PLoS pathogens · 2012Article
- Effect of ultrasound on herpes simplex virus infection in cell culture.Virology journal · 2011Article
- A novel fusogenic herpes simplex virus for oncolytic virotherapy of squamous cell carcinoma.Virology journal · 2011Article
- Gene therapy: the end of the rainbow?Head & neck oncology · 2009Review
- The effects of trichostatin A on the oncolytic ability of herpes simplex virus for oral squamous cell carcinoma cells.Cancer gene therapy · 2009Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current oncolytic viruses exert only limited antitumor activity on their own. There is a need to increase their oncolytic capability. We evaluated the effect of a differentiating reagent, hexamethylene bisacetamide (HMBA), on the antitumor activity of a gamma(1)34.5-deficient herpes simplex virus type 1 (HSV-1) R849 for human oral squamous cell carcinoma (SCC) cells. Hexamethylene bisacetamide increased the viral yield, especially at a low input multiplicity of infection (MOI), and the transcription of immediate early genes of HSV-1. Hexamethylene bisacetamide treatment promoted the cytopathic effect of R849 and increased the proportion of dead cells. Hexamethylene bisacetamide produced more apoptotic cells in R849-infected cells as compared with parental HSV-1(F)-infected cells. The growth of oral SCC xenografts in nude mice was markedly suppressed by treatment with R849 in combination with HMBA, and the survival of the co-treated animals was significantly prolonged as compared with that of animals treated with R849 only. Herpes simplex virus type 1 mRNA was expressed in tumors and trigeminal neurons, but not in brain, lung, liver, and kidney. These results indicate that HMBA enhances the antitumor activity of R849 through the expression of immediate early genes without increasing its toxicity. Hexamethylene bisacetamide can be used as an enhancing agent for oncolytic therapy with HSV-1 mutants.
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