The authors present a comprehensive review on the history and development of oncolytic herpes simplex viral therapies for malignant glioma with a focus on mechanisms of delivery in prior and ongoing clinical trials. This review highlights the advancements made with regard to delivering these therapies to a highly complex immunologic environment in the setting of the blood-brain and blood-tumor barrier in a safe and effective manner.
View Article and Find Full Text PDFDuring transcription, RNA polymerase II traverses through chromatin, and posttranslational modifications including histone methylations mark regions of active transcription. Histone protein H3 lysine 36 trimethylation (H3K36me3), which is established by the histone methyltransferase SET domain containing 2 (SETD2), suppresses cryptic transcription, regulates splicing, and serves as a binding site for transcription elongation factors. The mechanism by which the transcription machinery coordinates the deposition of H3K36me3 is not well understood.
View Article and Find Full Text PDFBackground: Neuroblastoma is the most common extracranial solid tumor in children and accounts for 15% of pediatric cancer related deaths. Targeting neuroblastoma with immunotherapies has proven challenging due to a paucity of immune cells in the tumor microenvironment and the release of immunosuppressive cytokines by neuroblastoma tumor cells. We hypothesized that combining an oncolytic Herpes Simplex Virus (oHSV) with natural killer (NK) cells might overcome these barriers and incite tumor cell death.
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