ArticleiScience2026
Targeting ADAR1 p150 triggers tumor inhibition and antitumor immunity to overcome immunotherapy resistance.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Targeting ADAR1 in Cancer: Biology, Therapeutic Strategies, Challenges, and Limitations.Pharmaceuticals (Basel, Switzerland) · 2026Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunotherapy efficacy is limited by resistance. While ADAR1 regulates tumor immune evasion, targeting it is challenged by the essential role of the constitutive p110 isoform. Here, we identify the interferon-inducible p150 isoform and its Zα domain as critical therapeutic vulnerabilities. ADAR1 p150 is frequently overexpressed in human cancers and correlates with immunosuppressive environments. Genetic ablation of p150 inhibits tumor proliferation and triggers a type I interferon response, converting "cold" tumors to "hot." Myeloid-specific ADAR1 deletion synergizes with anti-PD-1 therapy by enhancing antigen presentation. We establish the Zα domain as the essential determinant for dsRNA editing selectivity. Targeted disruption of this domain alone recapitulates the effects of complete ADAR1 ablation, leading to immunogenic dsRNA accumulation and potent anti-tumor immunity. This work provides a rationale for selectively targeting the ADAR1 p150-Zα axis to reverse malignant RNA editing and overcome immunotherapy resistance with a refined therapeutic index.
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Registered trials
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