ReviewMolecular biomedicine2026
Colitis-associated colorectal carcinogenesis: molecular mechanisms and therapeutic potential.
Review in Molecular biomedicine, 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
11 authors.
Funding
Abstract
Chronic colitis is a major risk factor for colorectal cancer (CRC), particularly for colitis-associated colorectal cancer (CAC), where persistent inflammation drives the transition from mucosal injury to malignant transformation. Accumulating evidence indicates that gut microbiota dysbiosis, epithelial barrier disruption, microbial translocation, chronic immune activation, and aberrant inflammatory signaling collectively contribute to CAC initiation and progression. Sustained inflammation promotes oxidative stress, DNA damage, genetic/epigenetic alterations, and tumor microenvironment remodeling, ultimately facilitating tumor development and immune evasion. These processes form an interconnected pathogenic network linking microbial, inflammatory, genetic, immune, and stromal alterations. This review comprehensively summarizes the key drivers and molecular mechanisms of CAC, covering microbiota and barrier dysfunction, inflammatory signaling, oxidative stress and DNA damage, genetic and epigenetic alterations, and tumor microenvironment remodeling and immune dysregulation. We further review recent advances in diagnostic biomarkers, disease monitoring, chemoprevention, targeted therapies, and emerging interventions, including the potential utility of specific chemokine axes as biomarkers and therapeutic targets. Particular emphasis is placed on the translational challenges of linking mechanistic insights to diagnostic and therapeutic advances, including biomarker validation, stage-specific interventions, and patient stratification across disease progression. By integrating these interconnected mechanisms and therapeutic strategies, this review provides a comprehensive framework for understanding CAC pathogenesis and identifies opportunities for precision prevention, early detection, and multimodal treatment.
Indexed as
Identifiers
42879037What 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.