CRISPR screens define unified hallmarks of cancer cell-autonomous immune evasion
- Author(s)
- Huber, A; Djajawi, TM; Rivera, IS; Vervoort, SJ; Kearney, CJ;
- Details
- Publication Year 2025-12-18,Volume 45,Issue #1,Page 116738
- Journal Title
- Cell Reports
- Abstract
- Cancer immunotherapy has transformed cancer treatment, yet only a minority of patients achieve durable benefit. Although early efforts to enhance immunotherapy focused on boosting immune effector function, reversing T cell exhaustion, or altering the tumor microenvironment, it is now clear that cancer cell-autonomous mechanisms play a major role in immune escape. Such programs, driven by the cancer cell genome, transcriptome, and epigenome, include desensitization to cytokine signaling, such as interferon (IFN)γ and tumor necrosis factor (TNF); impaired antigen presentation; upregulation of suppressive ligands such as programmed cell death ligand 1 (PD-L1); and epigenetic silencing of immunogenic pathways. The rise of high-throughput functional genomics, especially in vitro and in vivo CRISPR-based screening, has greatly expanded our ability to map these pathways and define how tumors evade CD8(+) T cell-mediated pressure. A deeper understanding of these cancer cell-autonomous immune-evasion mechanisms will be essential for developing new therapeutic strategies that broaden the impact of immunotherapy across diverse cancers.
- Publisher
- Cell Press
- Keywords
- CP: Cancer; CP: Immunology
- Research Division(s)
- Genetics and Gene Regulation
- PubMed ID
- 41417728
- Publisher's Version
- https://doi.org/10.1016/j.celrep.2025.116738
- Open Access at Publisher's Site
https://doi.org/10.1016/j.celrep.2025.116738- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2026-01-22 09:58:55
Last Modified: 2026-01-22 09:59:05