Component
Order of TET2 and JAK2 V617F acquisition in human myeloproliferative clones
Which lesion was present first in the same patient's haematopoietic clone.
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 defects were present in haematopoietic stem cells and preceded the JAK2 V617F mutation in the five analysed samples from patients with myeloproliferative disorders.
Experimental context and source evidence
- duration
- Cross-sectional
- experimental_model
- Five myeloproliferative-disorder patient samples with clonal analysis of progenitors
- exposure
- No intervention; clonal ordering within patient samples
- limitations
- Five samples. Order of acquisition in a clone does not by itself establish which lesion drives the disease.
- organism
- Homo sapiens
- plain_language
- Where both were present, the TET2 damage came first.
- primary_references
- [delhommeau-2009] Mutation in TET2 in myeloid cancers (2009). https://pubmed.ncbi.nlm.nih.gov/19474426/ DOI: 10.1056/nejmoa0810069
- tissue
- Haematopoietic stem and progenitor cells
TET2 loss and malignancy: the step between a nutrient-responsive enzyme and the disease (2026-09-23) · lines 23–31
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 · Five myeloproliferative-disorder patient samples with clonal analysis of progenitors · source_derived_draft · unverified_draft
## tet2-defect-precedes-jak2-v617f TET2 defects were present in haematopoietic stem cells and preceded the JAK2 V617F mutation in the five analysed samples from patients with myeloproliferative disorders. Model/species: Five myeloproliferative-disorder patient samples with clonal analysis of progenitors Organism: Homo sapiens Tissue/system: Haematopoietic stem and progenitor cells Exposure: No intervention; clonal ordering within patient samples Duration: Cross-sectional Limits: Five samples. Order of acquisition in a clone does not by itself establish which lesion drives the disease. Primary reference: [delhommeau-2009] Mutation in TET2 in myeloid cancers (2009). https://pubmed.ncbi.nlm.nih.gov/19474426/ DOI: 10.1056/nejmoa0810069
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.