ReviewTheranostics2026
STING signaling pathway: An oasis in the glioblastoma immune desert.
Review in Theranostics, 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
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
1 citing paper in PubMed.
- Review
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
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is an "immune desert" tumor, characterized by a highly immunosuppressive tumor microenvironment (TME), which leads to immune evasion and resistance to immunotherapies. The stimulator of interferon (IFN) genes (STING) signaling pathway serves as a central hub for priming anti-tumor immunity by driving the production of type I IFNs. Thus, STING activation has shown promise for overcoming immunosuppressive TME and inhibiting tumor malignancies. Accumulating preclinical evidence shows that STING agonists exert strong antitumor effects across multiple GBM models. However, the diverse and complex roles of the STING signaling pathway in reshaping the GBM microenvironment have not been fully summarized or elucidated. This review provides an overview of the mechanisms underlying STING dysregulation and the regulatory effect of STING activation on immune cell infiltration, priming, and function. Moreover, STING agonist monotherapies, and their combination regimens or delivery via innovative platforms for GBM treatment, are critically appraised, highlighting their implications for future clinical translation.
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Registered trials
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