ArticleCell reports. Medicine2026
Targeting RNase H2: A dual-mechanism strategy to elevate replication stress, DNA damage, and antitumor immunity in TNBC.
Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
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Who cites it
3 citing papers in PubMed.
- Immune response to DNA and RNA: structural insights, molecular mechanisms, and therapeutic targeting.Molecular biomedicine · 2026Review
- Emerging roles of RNA:DNA hybrid regulation by mammalian ribonuclease H2 in replication stress and cancer.Journal of cell science · 2025Review
- Drug Metabolism and Pharmacokinetic Evaluation of a Novel RNase H2 Inhibitor for the Treatment of Triple-Negative Breast Cancer.Pharmaceutics · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) lacks effective targeted therapies and carries a poor prognosis. TNBC cells escape oncogene-induced senescence and adapt to elevated replication stress. Here, we show that cells escaping senescence depend on overexpression of RNase H2, which removes misincorporated ribonucleotides from genomic DNA. RNASEH2A, the catalytic subunit of RNase H2, is overexpressed in TNBC tumors and correlates with poor survival. Genetic silencing or pharmacological inhibition of RNase H2 selectively impairs TNBC viability, spares non-tumorigenic mammary epithelial cells, and suppresses tumor growth in vivo. Mechanistically, RNase H2 inhibition increases replication stress, DNA damage, and cytosolic single-stranded DNA accumulation, triggering innate immune activation and upregulation of T cell-recruiting chemokines. RNase H2 inhibition synergizes with ATR and PARP inhibitors and enhances immune checkpoint blockade efficacy. Together, these findings identify RNase H2 as a therapeutic vulnerability in TNBC and support combined strategies integrating DNA damage modulation and immunotherapy.
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Registered trials
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