Component
TET2 mutation in human lymphoid neoplasms
TET2 mutations detected in lymphoid disorders, reported alongside the mouse work in the same study.
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
TET2 mutations were observed in human lymphoid disorders and could be detected in immature progenitors that retained myeloid colony-forming potential.
Experimental context and source evidence
- duration
- Cross-sectional
- experimental_model
- Human lymphoid disorder samples with progenitor colony assays
- exposure
- No intervention; observational sequencing
- limitations
- Detection in a progenitor shows where the mutation sits in the hierarchy, not that it caused the lymphoid tumour.
- organism
- Homo sapiens
- plain_language
- The same damaged gene also turns up in lymphoid cancers, not only myeloid ones.
- primary_references
- [quivoron-2011] TET2 inactivation results in pleiotropic hematopoietic abnormalities in mouse and is a recurrent event during human lymphomagenesis (2011). https://pubmed.ncbi.nlm.nih.gov/21723201/ DOI: 10.1016/j.ccr.2011.06.003
- tissue
- Lymphoid tumour cells and immature progenitors
TET2 loss and malignancy: the step between a nutrient-responsive enzyme and the disease (2026-09-23) · lines 83–91
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 · Human lymphoid disorder samples with progenitor colony assays · source_derived_draft · unverified_draft
## tet2-mutation-in-lymphoid-disorders TET2 mutations were observed in human lymphoid disorders and could be detected in immature progenitors that retained myeloid colony-forming potential. Model/species: Human lymphoid disorder samples with progenitor colony assays Organism: Homo sapiens Tissue/system: Lymphoid tumour cells and immature progenitors Exposure: No intervention; observational sequencing Duration: Cross-sectional Limits: Detection in a progenitor shows where the mutation sits in the hierarchy, not that it caused the lymphoid tumour. Primary reference: [quivoron-2011] TET2 inactivation results in pleiotropic hematopoietic abnormalities in mouse and is a recurrent event during human lymphomagenesis (2011). https://pubmed.ncbi.nlm.nih.gov/21723201/ DOI: 10.1016/j.ccr.2011.06.003
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.