ReviewClinical and translational medicine2026
Stimulator of interferon genes (STING)-activating nanomedicines: Translating innate immune modulation into effective therapy for triple-negative breast cancer.
Review in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed.
- Current Perspectives on STING Agonists for Anticancer Drug Development.Chemical biology & drug design · 2026Review
- Stimulator of interferon genes (STING)-activating nanomedicines: Translating innate immune modulation into effective therapy for triple-negative breast cancer.Clinical and translational medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC), marked by profound immunosuppressive complexity, poses a critical challenge in therapy due to the absence of hormone receptors in its phenotype, making it unavailable for conventional therapies. The stimulator of interferon genes (STING) pathway is emerging as critical pathway translating the immunogenic 'cold' TNBC tumour into 'hot' one, thereby improving the responsiveness to immune checkpoint blockade (ICB). However, the clinical translation is still hindered by insufficient cytosolic delivery, rapid systemic degradation and tumour microenvironment-induced metabolic inactivation. This review outlines the recent advances in STING-mediated nanoparticle delivery with special emphasis on biomimetic, Trojan horse logic gate, manganese-based and redox-responsive stimuli delivery systems. Mechanistically, it integrates immune activation by ferroptosis, cuproptosis and mitochondrial DNA disruption. They synergise the amplification of type 1 interferon with dendritic cell maturation, potentiating antitumour immunogenesis. Notably, the combination with ICBs will further amplify the therapeutic potential of nanoparticles. Convergence of immunology and targeted therapies with nanoparticles opens new array for TNBC treatment. The review visualizes the clinical translation of mind maps into clinical reality, activating the innate immunity. HIGHLIGHTS: STING activation converts immunologically cold TNBC into ICB-responsive hot tumors. Nanoparticles overcome poor delivery, degradation, and TME-driven STING inactivation. Biomimetic and stimuli-responsive systems enhance type I IFN and DC maturation. Synergy with ICBs boosts innate immunity and antitumor immunogenesis.
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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 Socratic graph.