ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Interferon-Driven Biomarkers and Synergistic Therapy for PRMT5 Inhibition in Triple-Negative Breast Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
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
4 citing papers in PubMed.
- The dual immune landscape of homologous recombination-deficient tumors: mechanisms and therapeutic implications.Cancer metastasis reviews · 2026Review
- PRMT5 as a Key Driver of Stemness and Metastatic Potential in Triple-Negative Breast Cancer.Biomolecules · 2026Review
- Focused ultrasound for cellular mechanoactivation and nanomedicine delivery in cancer.Biomedical microdevices · 2026Review
- Interferon-Driven Biomarkers and Synergistic Therapy for PRMT5 Inhibition in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) exhibits heterogeneous responses to PRMT5 inhibition, posing challenges for therapeutic targeting. Here, using PRMT5 inhibitors, coupled with transcriptomic profiling, basal interferon (IFN) signaling is identified as a biomarker of PRMT5 inhibition sensitivity. Sensitive TNBC models are characterized by elevated DNA damage, which correlated with enriched IFN pathway activity. Pharmacologically inducing DNA damage with the PARP inhibitor Olaparib activated IFN signaling and synergistically sensitized resistant TNBC cells to PRMT5 inhibition. Comprehensive pre-clinical validation in patient-derived organoid (PDO) and xenograft (PDX) models demonstrated robust antitumor efficacy of this combination therapy. Moreover, this dual targeting strategy reshaped the tumor microenvironment, enhancing dendritic cell-CD8
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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.