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Effect of SOCS1 overexpression on AML gene expression in OCI-AML2 cell line

GSE288632 Homo sapiens Expression profiling by high throughput sequencing 4 samples Submitted 2025/02/08 Platform GPL24676
Summary
Despite the curative potential of allogeneic hematopoietic stem cell transplantation for acute myeloid leukemia (AML), its efficacy is limited by intrinsic resistance of cancer cells to donor-derived T-cell cytotoxicity. Using a genome-wide CRISPR screen, we identified the SOCS1-JAK1-STAT1 pathway as a mediator of AML susceptibility to T cells. SOCS1 knockdown in AML cells sensitized them to killing by allogeneic T cells, whereas SOCS1 overexpression in AML cells induced resistance to T-cell anti-leukemic activity. Mechanistically, SOCS1 protected AML cells from T-cell killing by antagonizing IFNγ-JAK1-induced ICAM-1 expression. Furthermore, primary AML cells with lower SOCS1 expression correlated with better overall survival in patients, especially those with a lower exhausted CD8+ T-cell score. Thus, this study reveals SOCS1 and its downstream mediators as a potential targetable pathway to enhance T cell-based immunotherapy for AML.
Published in
SOCS1 Protects Acute Myeloid Leukemia against Allogeneic T Cell-Mediated Cytotoxicity
Tin E, Rutella S, Khatri I et al. · Blood cancer discovery 2025 · PMID 39928733 · doi:10.1158/2643-3230.BCD-24-0140
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Direct links to NCBI, no account and no request form: the whole study as GSE288632_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 PRJNA1218726 and SRA study SRP561306. Searching any of these in the dataset finder brings you back here.

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