ArticleeLife2019
Systematic identification of cancer cell vulnerabilities to natural killer cell-mediated immune surveillance.
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Disrupting Mechanisms that Regulate Genomic Repeat Elements to Combat Cancer and Drug Resistance.Frontiers in cell and developmental biology · 2022Pooled it
- Anti-BCMA CAR-NK Cells Reveal Enhanced Cytolytic and Secretory Responses Against Myeloma Cells.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2026Article
- Surfaceome CRISPR activation screening uncovers ligands regulating tumor sensitivity to NK cell killing.Nature communications · 2026Article
- BAP1 loss impairs IFN-γ signaling and enhances NK cell-mediated cytotoxicity in myeloid leukemia.Cancer immunology, immunotherapy : CII · 2026Article
- Multiplexed perturbation enables scalable pooled screens.Nature methods · 2026Article
- DUSP6 ablation restores CAR T-cell fitness impaired by tumor CD58 loss through invigoration of AP-1 signaling.Signal transduction and targeted therapy · 2026Article
- Functional genomics-guided design of CAR-T and CAR-NK therapies in hematological malignancies: aligning cellular engineering with immune escape and microenvironmental resistance.Frontiers in genome editing · 2026Review
- The Activity of EGFR CAR NK and CAR T Cells against EGFR Inhibitor-Resistant NSCLC and Drug-Tolerant Persister Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- RBM39 degrader invigorates innate immunity to eradicate neuroblastoma despite cancer cell plasticity.Nature communications · 2025Article
- Exploitable mechanisms of antibody and CAR mediated macrophage cytotoxicity.Nature communications · 2025Article
- Genome-wide CRISPR/Cas9 screen reveals factors that influence the susceptibility of tumor cells to NK cell-mediated killing.Journal for immunotherapy of cancer · 2025Article
- Potentiating anti-tumor immunity by re-engaging immune synapse molecules.Cell reports. Medicine · 2025Article
- Integrating artificial intelligence in drug discovery and early drug development: a transformative approach.Biomarker research · 2025Review
- Evolutionary trajectories of immune escape across cancers.bioRxiv : the preprint server for biology · 2025Article
- SMARCA4 regulates the NK-mediated killing of senescent cells.Science advances · 2025Article
- The present and future of the Cancer Dependency Map.Nature reviews. Cancer · 2025Review
- A potential prognostic marker for hematologic neoplasms: CD58.Frontiers in oncology · 2025Review
- Engineering immune-evasive allogeneic cellular immunotherapies.Nature reviews. Immunology · 2024Review
- DCAF15 control of cohesin dynamics sustains acute myeloid leukemia.Nature communications · 2024Article
- IFNγ mediates the resistance of tumor cells to distinct NK cell subsets.Journal for immunotherapy of cancer · 2024Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Only a subset of cancer patients respond to T-cell checkpoint inhibitors, highlighting the need for alternative immunotherapeutics. We performed CRISPR-Cas9 screens in a leukemia cell line to identify perturbations that enhance natural killer effector functions. Our screens defined critical components of the tumor-immune synapse and highlighted the importance of cancer cell interferon-γ signaling in modulating NK activity. Surprisingly, disrupting the ubiquitin ligase substrate adaptor DCAF15 strongly sensitized cancer cells to NK-mediated clearance. DCAF15 disruption induced an inflamed state in leukemic cells, including increased expression of lymphocyte costimulatory molecules. Proteomic and biochemical analysis revealed that cohesin complex members were endogenous client substrates of DCAF15. Genetic disruption of DCAF15 was phenocopied by treatment with indisulam, an anticancer drug that functions through DCAF15 engagement. In AML patients, reduced DCAF15 expression was associated with improved survival. These findings suggest that DCAF15 inhibition may have useful immunomodulatory properties in the treatment of myeloid neoplasms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.