Component
TET2 mutation frequency across human myeloid neoplasms
The proportion of patients in a sequenced series carrying a somatic TET2 deletion or mutation.
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
Sequencing the TET2 coding region in 320 patients found somatic deletions or mutations in 19% of myelodysplastic syndromes (15 of 81), 12% of myeloproliferative disorders (24 of 198), 24% of secondary acute myeloid leukaemia (5 of 21) and 22% of chronic myelomonocytic leukaemia (2 of 9).
Experimental context and source evidence
- duration
- Cross-sectional
- experimental_model
- 320 patients with myeloid cancers; molecular, cytogenetic, comparative-genomic-hybridization and SNP analyses
- exposure
- No intervention; observational sequencing of patient material
- limitations
- A mutation frequency is an association, not a demonstration that TET2 loss caused any of these cancers. Ascertainment was partly enriched: six patients were selected for 4q24 rearrangements and five for a JAK2 V617F-positive dominant clone.
- organism
- Homo sapiens
- plain_language
- About one in seven patients with these blood cancers carried a damaged copy of TET2.
- primary_references
- [delhommeau-2009] Mutation in TET2 in myeloid cancers (2009). https://pubmed.ncbi.nlm.nih.gov/19474426/ DOI: 10.1056/nejmoa0810069
- tissue
- Haematopoietic cells and bone marrow
TET2 loss and malignancy: the step between a nutrient-responsive enzyme and the disease (2026-09-23) · lines 13–21
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 · 320 patients with myeloid cancers; molecular, cytogenetic, comparative-genomic-hybridization and SNP analyses · source_derived_draft · unverified_draft
## tet2-mutated-across-myeloid-neoplasms Sequencing the TET2 coding region in 320 patients found somatic deletions or mutations in 19% of myelodysplastic syndromes (15 of 81), 12% of myeloproliferative disorders (24 of 198), 24% of secondary acute myeloid leukaemia (5 of 21) and 22% of chronic myelomonocytic leukaemia (2 of 9). Model/species: 320 patients with myeloid cancers; molecular, cytogenetic, comparative-genomic-hybridization and SNP analyses Organism: Homo sapiens Tissue/system: Haematopoietic cells and bone marrow Exposure: No intervention; observational sequencing of patient material Duration: Cross-sectional Limits: A mutation frequency is an association, not a demonstration that TET2 loss caused any of these cancers. Ascertainment was partly enriched: six patients were selected for 4q24 rearrangements and five for a JAK2 V617F-positive dominant clone. 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.