ReviewDiscover oncology2025
Deciphering the metabolic landscape of colorectal cancer through the lens of AhR-mediated intestinal inflammation.
Review in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Therapeutic Efficacy of Carvacrol-Loaded Mesoporous Silicate Nanoparticles Against Cryptosporidiosis.Pharmaceutics · 2026Article
- From Microbiota to Defense: The Preventive Effect and Mechanism of Total Flavonoids from Sea Buckthorn Leaves in DSS-Induced Colitis.Nutrients · 2026Article
- Cell Line-Dependent Cell Death Pathways Induced by Thymoquinone in Colorectal Cancer Cells.Molecules (Basel, Switzerland) · 2026Article
- Context-dependent functions of the aryl hydrocarbon receptor in gastrointestinal cancers: from microenvironmental regulation to precision targeted therapy.Frontiers in cell and developmental biology · 2026Review
- Time-Dependent Impact of Betulin and Its Derivatives on IL-8 Expression in Colorectal Cancer Cells with Molecular Docking Studies.International journal of molecular sciences · 2025Article
- Article
- Association of MMP-11 Genotypes With Colorectal Cancer in Taiwan.In vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Colorectal cancer (CRC) ranks as the third most common cancer worldwide, with its incidence steadily increasing due to an aging demographic and various lifestyle-related risk factors, including poor nutrition, tobacco use, sedentary behaviour and obesity. These factors promote the risk of colorectal cancer by inducing chronic colonic inflammation, a principal catalyst of carcinogenesis. This review delves into evidence that suggests that metabolic abnormalities mediated through inflammatory responses are fundamental in the progression of CRC. This dysregulation of essential metabolic pathways in colorectal cancer, facilitates tumor proliferation, immune evasion, and metastasis. Additionally, this review explores how inflammatory mediators, and dietary carcinogens induce metabolic alterations, fostering a pro-tumorigenic milieu. Special focus is placed on the aryl hydrocarbon receptor (AhR) as a pivotal metabolic regulator that links inflammation and tumor metabolism, elucidating its function in the reconfiguration of cellular energetics and the inflammatory microenvironment. Furthermore, this review also focuses on clarifying the relationship between inflammation, metabolic dysregulation, and the progression of CRC, so as to identify potential therapeutic targets.
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Identifiers
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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.