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An Irf2-expressing oncolytic virus changes the susceptibility of tumor to antitumor T cells and promotes promotes tumor clearance

GSE261564 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2024/03/18 Platform GPL19057
Summary
According to our previous studies, IRF1-deficient (IRF1-KO) tumor cells showed significantly reduced tumor growth when injected in several syngeneic mouse models including the B16-F10 melanoma, indicating that tumor cells require IRF1 for sustained tumor progression. Depletion of CD8+ T cells or NK cells could restore tumor growth of IRF1-KO cells. In addition, we found that loss of IRF1 in tumor cells could decrease the IFNγ-induced expression of PD-L1. To examine if IRF1 can be a target for cancer immunotherapy, we attempted to comprehensively identify genes that are specifically regulated by IRF1 in tumor cells that contribute to the tumor progression and the suppression of immune surveillance. Our RNA-seq data suggest that IRF1 regulates not only the expression of immune inhibitory ligands, but also the production of class I MHC molecules.
Published in
An IRF2-Expressing Oncolytic Virus Changes the Susceptibility of Tumor Cells to Antitumor T Cells and Promotes Tumor Clearance
Shao L, Srivastava R, Delgoffe GM et al. · Cancer immunology research 2024 · PMID 38517470 · doi:10.1158/2326-6066.CIR-23-0573
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Direct links to NCBI, no account and no request form: the whole study as GSE261564_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 4 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1087454 and SRA study SRP495127. Searching any of these in the dataset finder brings you back here.

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