ReviewJournal of gastrointestinal cancer2026
cGAS-STING Pathway in Gastrointestinal Malignancies: Mechanistic Insights and Translational Therapeutic Opportunities.
Review in Journal of gastrointestinal cancer, 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.
- Sex Differences in Mitochondrial Function: Endocrine Regulation, Immunometabolic Signaling, and Implications for Health and Disease.International journal of molecular sciences · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAn important regulator of tumor immunosurveillance and innate immune activation in gastrointestinal (GI) malignancies is the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway. The release of type I interferons, dendritic cell (DC) maturation, and cytotoxic T lymphocyte recruitment are the final steps of a pathway that is typically set in motion by aberrant DNA damage, microbiome-derived DNA, or mitochondrial stress.
methodsTumour has it that immunologically "cold" gastrointestinalcancers can be made more sensitive to immune-checkpoint blockade (ICB), radiation, and chemotherapy by therapeutically activating the cGAS-STING pathway, which turns them into inflamed, T-cell-permissive niches.
resultsProgress in nanomedicine, small-molecule STING agonists, and tumour-microenvironment-responsive drug delivery systems has broadened the translational scope of this pathway across colorectal, gastric, and pancreatic malignancies. However, tumour-intrinsic heterogeneity, the dual immunostimulatory and immunosuppressive functions of chronic STING signalling, and delivery-related toxicities continue to pose substantial challenges.
conclusionThis review consolidates current mechanistic insights, preclinical evidence, and emergent clinical data regarding the cGAS-STING pathway in gastrointestinal cancers, while emphasising biomarker-guided patient stratification and AI-powered predictive tools that could facilitate the precise application of STING-targeted therapies.
Indexed as
Identifiers
41655160What 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.