ArticleFrontiers in genetics2026
Genomic and transcriptomic insights into aflatoxin-induced intrahepatic cholangiocarcinoma: an integrated pathway and meta-analysis study.
Article in Frontiers in genetics, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Environmental and chemical exposures are major yet incompletely characterized drivers of human carcinogenesis. Aflatoxin, a potent food-borne mycotoxin, has been implicated in tumor initiation, proliferation, and immune suppression in intrahepatic cholangiocarcinoma (ICC), but its genomic mechanisms remain poorly defined. Methods: We employed extensive literature data mining (LDM) to identify genes associated with both aflatoxin exposure and ICC, enabling construction of a mechanistic genetic pathway linking exposure to disease. These pathways were further evaluated using a meta-analysis of five Gene Expression Omnibus (GEO) expression datasets, followed by functional annotation to characterize their biological roles. Results: LDM identified 1,754 ICC-associated genes, of which 427 were also linked to aflatoxin, with 154 positioned as potential intermediate regulators connecting aflatoxin exposure to ICC. Meta-analysis revealed significant expression alterations in six genes upon aflatoxin exposure, including upregulation of CRP, CDK2, AXL, and MIR221 (overexpression >50%, p < 0.05) and downregulation of F2 and BUB1B (reduced expression >60%, p < 0.014). Co-expression analysis indicated strong interactions among these regulators (Fisher's Z > 0.53, p < 0.05), suggesting coordinated molecular responses associated with ICC progression. Functional annotation further highlighted inflammatory responses, cytokine dysregulation, and kinase-related signaling as key processes potentially linking aflatoxin exposure to ICC development. Discussion: These findings provide a systems-level view of the genomic mechanisms underlying aflatoxin-associated ICC carcinogenesis and identify candidate molecular mediators linking environmental toxin exposure to tumor development. This integrative framework may facilitate exposure-informed biomarker discovery and potential preventive or therapeutic strategies, particularly in regions where aflatoxin exposure remains prevalent.
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.