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Showing 1–5 of 5 results
Advanced filters: Author: Laura Evgin Clear advanced filters

  • DNA mutations induced by dysregulated APOBEC3 expression are associated with tumour-progression and therapeutic resistance, but also with the generation of neoepitopes. Here, the authors show that APOBEC3 function can be exploited in a vaccine setting to generate heteroclitic neoepitopes, enhancing sensitivity to immunotherapy.

    • Christopher B. Driscoll
    • Matthew R. Schuelke
    • Richard G. Vile
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-14

  • Oncolytic viruses promote an inflammatory response and elicit anti-tumor immunity. Here the authors show, unexpectedly, that the oncolytic virus, VSVIFNβ, induces type I interferon responses that, when combined with chimeric antigen receptor (CAR) T therapy, lead to the attrition of both CAR T and conventional T cells, thus dampening their anti-tumor activity.

    • Laura Evgin
    • Amanda L. Huff
    • Richard Vile
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-15

  • Oncolytic viruses create an inflamed tumour microenvironment allowing T cells to respond to immune checkpoint blockade therapy more efficiently. Authors here show that in a hepatocellular carcinoma model, a dominant anti-viral rather than anti-tumour T cell response is elicited by an oncolytic vesicular stomatitis virus, unless the virus is designed to express tumour antigens, which restores therapeutic benefit.

    • Mason J. Webb
    • Thanich Sangsuwannukul
    • Richard Vile
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-18

  • Oncolytic viruses, such as vesicular stomatitis virus (VSV), are a promising class of cancer therapeutics. Here the authors report that a mutation in the CSDE1 gene renders cancer cells resistant to VSV replication and oncolysis, but a mutation-derived escape-associated neoantigen could be exploited for immunotherapy against treatment-resistant tumors.

    • Timothy Kottke
    • Jason Tonne
    • Richard G. Vile
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-15