ArticleOncogene2026
Synergistic reprogramming of the tumor immune microenvironment by Senecavirus A and STING agonist.
Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stimulator of interferon genes (STING) agonists have shown promise in cancer immunotherapy by enhancing type I interferon (IFN-I) signaling. However, the antiviral effects of IFN-I can suppress viral replication, limiting their combination with oncolytic viruses. This study demonstrates that combining a naturally isolated Senecavirus A (SVA) strain with the STING agonist MSA-2 supports synergistic IFN-I activation across multiple tumor models. The combination induces robust innate and adaptive antitumor immune responses without impairing SVA replication. Transcriptomics, immunoblotting and early IRF7 nuclear translocation in B16‑F10 cells are consistent with engagement of the RIG‑I/MDA5-TBK1-IRF7 axis. In vivo, co‑treatment enhanced IFN‑β induction, increased CD8⁺ T‑cell infiltration and reduced tumor burden relative to monotherapies, whereas efficacy was not observed in athymic nude mice, supporting T‑cell dependence. Together, these data provide preclinical evidence that a rational oncolytic virus and STING combination can amplify antitumor immunity without overtly compromising viral persistence.
Indexed as
Identifiers
41673092What OpenQuestion holds
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.