ReviewFrontiers in immunology2026
The microbiota-metabolite-immune axis in colorectal cancer: mechanistic insights and emerging clinical applications.
Review in Frontiers in immunology, 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.
- Interkingdom microbiome physiology in colorectal cancer: barrier dysfunction, immune-metabolic signaling, and therapeutic resistance.Frontiers in physiology · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) results from a complex interplay of host genetics, environmental factors, and gut microbiota. Increasing evidence suggests that intestinal microorganisms significantly affect the initiation and progression of CRC through metabolic and immunological reprogramming. Dysbiosis, defined as an imbalance between beneficial and harmful microbial species, leads to chronic inflammation, genotoxic stress, and disruption of epithelial homeostasis. Microbial metabolites, such as short-chain fatty acids, secondary bile acids, and tryptophan derivatives, function as signaling molecules that influence epithelial proliferation, apoptosis, and immune cell activity. These metabolites regulate essential oncogenic and inflammatory pathways, including Wnt/β-catenin, NF-κB, and STAT3, and alter the tumor microenvironment by affecting regulatory T cells (Tregs), Th17 cells, macrophages, and myeloid-derived suppressor cells. Specific bacteria, such as
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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 OpenQuestion graph.