ArticleJournal of biomedical science2026
A STING signaling relay from tumor cells to macrophages mediates the improved efficacy of combination chemotherapy in pancreatic cancer.
Article in Journal of biomedical science, 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.
- STING agonist profiling by nucleotide library defines structural determinants of cyclic dinucleotide recognition.iScience · 2026Article
- Efficacy of immune checkpoint inhibitors combined with different chemotherapy in recurrent pancreatic cancer: a retrospective study.Frontiers in immunology · 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
15 authors.
Funding
Abstract
backgroundThe therapeutic efficacy of traditional chemotherapy on pancreatic ductal adenocarcinoma (PDAC) remains dismal. In this study, we investigated the efficacy of adding cisplatin to the standard first-line gemcitabine plus nab-paclitaxel (AG) regimen (referred to as AGP) for PDAC treatment, and elucidated the underlying mechanisms, particularly the role of the cGAS-STING pathway in mediating chemotherapy-induced antitumor immunity in PDAC.
methodsWe first reported the therapeutic efficacy of an AGP regimen in patients with PDAC through a clinical retrospective analysis. Next, we mimicked the enhanced efficacy of the AGP regimen in both subcutaneous and orthotopic PDAC mouse models. Comprehensive immune profiling was performed using mass cytometry, flow cytometry, multiplex immunofluorescence, and RNA sequencing to characterize changes in immune cell populations and phenotypes. The functional significance of the cGAS-STING pathway was investigated through genetic ablation of tumor cells and macrophages. Tumor-macrophage interactions were further explored via co-culture assays. Clinical relevance was assessed through a retrospective analysis of cohorts of patients with PDAC and immunohistochemical evaluation of STING expression in tumor tissues.
resultsThe AGP regimen confers promising potential to AG regimen in patients with PDAC as well as in PDAC mouse models. Mechanistically, cisplatin-induced DNA damage in tumor cells activated the tumor-intrinsic cGAS-STING pathway, which facilitated the recruitment and activation of CD8
conclusionsThis study reports AGP regimen as a promising therapeutic modality for PDAC, and provides a detailed mechanism by which a STING-mediated signaling relay from PDAC tumor cells to TAMs boost antitumor immunity and contribute to AGP chemotherapy efficacy. Furthermore, STING expression in tumor tissues correlated with improved prognosis, highlighting its potential as a predictive biomarker and promising therapeutic target.
Indexed as
Identifiers
What 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.