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    IFN-gamma is required for cytotoxic T cell-dependent cancer genome immunoediting

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    Author
    Takeda, K; Nakayama, M; Hayakawa, Y; Kojima, Y; Ikeda, H; Imai, N; Ogasawara, K; Okumura, K; Thomas, DM; Smyth, MJ
    Date
    2017-02-24
    Source Title
    Nature Communications
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Thomas, David
    Affiliation
    Sir Peter MacCallum Department of Oncology
    Metadata
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    Document Type
    Journal Article
    Citations
    Takeda, K., Nakayama, M., Hayakawa, Y., Kojima, Y., Ikeda, H., Imai, N., Ogasawara, K., Okumura, K., Thomas, D. M. & Smyth, M. J. (2017). IFN-gamma is required for cytotoxic T cell-dependent cancer genome immunoediting. NATURE COMMUNICATIONS, 8 (1), https://doi.org/10.1038/ncomms14607.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/258195
    DOI
    10.1038/ncomms14607
    Abstract
    Genetic evolution that occurs during cancer progression enables tumour heterogeneity, thereby fostering tumour adaptation, therapeutic resistance and metastatic potential. Immune responses are known to select (immunoedit) tumour cells displaying immunoevasive properties. Here we address the role of IFN-γ in mediating the immunoediting process. We observe that, in several mouse tumour models such as HA-expressing 4T1 mammary carcinoma cells, OVA-expressing EG7 lymphoma cells and CMS5 MCA-induced fibrosarcoma cells naturally expressing mutated extracellular signal-regulated kinase (ERK) antigen, the action of antigen-specific cytotoxic T cell (CTL) in vivo results in the emergence of resistant cancer cell clones only in the presence of IFN-γ within the tumour microenvironment. Moreover, we show that exposure of tumours to IFN-γ-producing antigen-specific CTLs in vivo results in copy-number alterations (CNAs) associated with DNA damage response and modulation of DNA editing/repair gene expression. These results suggest that enhanced genetic instability might be one of the mechanisms by which CTLs and IFN-γ immunoedits tumours, altering their immune resistance as a result of genetic evolution.

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