Component
Bone-marrow genomic 5-hydroxymethylcytosine content
Measured 5hmC in genomic DNA from patient bone marrow.
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
Bone marrow from patients carrying TET2 mutations showed uniformly low 5-hydroxymethylcytosine in genomic DNA compared with bone marrow from healthy controls, and the mutations compromised catalytic activity in the same study.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- duration
- Cross-sectional
- experimental_model
- Patient bone-marrow samples with and without TET2 mutations; catalytic assays of mutant protein
- exposure
- No intervention; naturally occurring mutations
- limitations
- Samples with low 5hmC showed hypomethylation relative to controls at the majority of differentially methylated CpG sites, so the downstream methylation consequence is not a simple global gain.
- organism
- Homo sapiens
- plain_language
- Patients with a damaged TET2 had less of the chemical mark the enzyme makes.
- primary_references
- [ko-2010] Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2 (2010). https://pubmed.ncbi.nlm.nih.gov/21057493/ DOI: 10.1038/nature09586
- tissue
- Bone marrow genomic DNA
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
TET2 loss and malignancy: the step between a nutrient-responsive enzyme and the disease (2026-09-23) · lines 33–41
Original AI-assisted curation of twelve primary studies located by Europe PMC title search, with every statement drafted from the retrieved abstract. Two pairs share a laboratory and are recorded as one line of evidence each. Genetic loss of function, pharmacological exposure and dietary depletion are kept as separate record types. Not publisher full text. · supports · Patient bone-marrow samples with and without TET2 mutations; catalytic assays of mutant protein · source_derived_draft · unverified_draft
## tet2-mutation-lowers-marrow-5hmc Bone marrow from patients carrying TET2 mutations showed uniformly low 5-hydroxymethylcytosine in genomic DNA compared with bone marrow from healthy controls, and the mutations compromised catalytic activity in the same study. Model/species: Patient bone-marrow samples with and without TET2 mutations; catalytic assays of mutant protein Organism: Homo sapiens Tissue/system: Bone marrow genomic DNA Exposure: No intervention; naturally occurring mutations Duration: Cross-sectional Limits: Samples with low 5hmC showed hypomethylation relative to controls at the majority of differentially methylated CpG sites, so the downstream methylation consequence is not a simple global gain. Primary reference: [ko-2010] Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2 (2010). https://pubmed.ncbi.nlm.nih.gov/21057493/ DOI: 10.1038/nature09586
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.