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- W3138833517 abstract "Abstract In our clinical trials of oncolytic vesicular stomatitis virus expressing interferon beta (VSV-IFNβ), several patients achieved initial responses followed by aggressive relapse. We show here that VSV-IFNβ-escape tumors predictably express a point-mutated CSDE1 P5S form of the RNA-binding Cold Shock Domain-containing E1 protein, which promotes escape as an inhibitor of VSV replication by disrupting viral transcription. Given time, VSV-IFNβ evolves a compensatory mutation in the P / M Inter-Genic Region which rescues replication in CSDE1 P5S cells. These data show that CSDE1 is a major cellular co-factor for VSV replication. However, CSDE1 P5S also generates a neo-epitope recognized by non-tolerized T cells. We exploit this predictable neo-antigenesis to drive, and trap, tumors into an escape phenotype, which can be ambushed by vaccination against CSDE1 P5S , preventing tumor escape. Combining frontline therapy with escape-targeting immunotherapy will be applicable across multiple therapies which drive tumor mutation/evolution and simultaneously generate novel, targetable immunopeptidomes associated with acquired treatment resistance." @default.
- W3138833517 created "2021-03-29" @default.
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- W3138833517 date "2021-03-26" @default.
- W3138833517 modified "2023-10-17" @default.
- W3138833517 title "Oncolytic virotherapy induced CSDE1 neo-antigenesis restricts VSV replication but can be targeted by immunotherapy" @default.
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- W3138833517 doi "https://doi.org/10.1038/s41467-021-22115-1" @default.
- W3138833517 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7997928" @default.
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- W3138833517 hasPublicationYear "2021" @default.
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