Component
Proliferation of Apc/Msh2-deficient mouse colonic epithelium
Context-specific entity; species, compartment and exposure are stated on each claim.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Carbohydrate-derived microbial metabolites including butyrate fueled hyperproliferation of Msh2-deficient colonic epithelium in the Apc-mutant mouse cancer model.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Apc-mutant/Msh2-deficient mice; dietary and microbial perturbation.
- limitations
- Genotype-specific model, not proof that butyrate causes cancer in healthy humans or that fiber should be avoided. Correction record: A published erratum is confirmed by PubMed and publisher/Crossref metadata: Cell 159(2):456, 2014. The notice body was not available through the accessed publisher endpoints, so its specific impact has not been assessed. The abstract-based MSH2 claim remains provisional with this unresolved correction flag. https://doi.org/10.1016/j.cell.2014.09.041
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- A genetically altered epithelium could use the metabolite to support abnormal growth.
- primary_references
- Gut microbial metabolism drives transformation of MSH2-deficient colon epithelial cells. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25036629/ · DOI 10.1016/j.cell.2014.04.051
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 638–644
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Apc-mutant/Msh2-deficient mice; dietary and microbial perturbation. · source_derived_draft · unverified_draft
## butyrate-msh2-context A genetically altered epithelium could use the metabolite to support abnormal growth. Carbohydrate-derived microbial metabolites including butyrate fueled hyperproliferation of Msh2-deficient colonic epithelium in the Apc-mutant mouse cancer model. Model: Apc-mutant/Msh2-deficient mice; dietary and microbial perturbation. Limitations: Genotype-specific model, not proof that butyrate causes cancer in healthy humans or that fiber should be avoided. Correction record: A published erratum is confirmed by PubMed and publisher/Crossref metadata: Cell 159(2):456, 2014. The notice body was not available through the accessed publisher endpoints, so its specific impact has not been assessed. The abstract-based MSH2 claim remains provisional with this unresolved correction flag. https://doi.org/10.1016/j.cell.2014.09.041 Evidence access: Primary abstract Gut microbial metabolism drives transformation of MSH2-deficient colon epithelial cells. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25036629/ · DOI 10.1016/j.cell.2014.04.051
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.