Component
Human acute myeloid leukaemia colony formation and xenograft progression
Leukaemic colony formation in vitro and leukaemia progression in patient-derived xenografts.
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
Vitamin C treatment suppressed leukaemic colony formation by human leukaemia cells and slowed leukaemia progression in primary human acute-myeloid-leukaemia patient-derived xenografts.
Experimental context and source evidence
- duration
- Colony assays and xenograft progression
- experimental_model
- Human leukaemia cell lines and primary human AML patient-derived xenografts
- exposure
- Pharmacological vitamin C
- limitations
- Pharmacological vitamin C in a xenograft is not dietary intake, and a xenograft host lacks an intact immune system.
- organism
- Homo sapiens cells in mouse xenograft hosts
- plain_language
- Vitamin C slowed human leukaemia cells in a dish and in mice carrying them.
- primary_references
- [cimmino-2017] Restoration of TET2 function blocks aberrant self-renewal and leukemia progression (2017). https://pubmed.ncbi.nlm.nih.gov/28823558/ DOI: 10.1016/j.cell.2017.07.032
- tissue
- Leukaemic blasts
TET2 loss and malignancy: the step between a nutrient-responsive enzyme and the disease (2026-09-23) · lines 113–121
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 leukaemia cell lines and primary human AML patient-derived xenografts · source_derived_draft · unverified_draft
## ascorbate-suppresses-aml-colony-formation Vitamin C treatment suppressed leukaemic colony formation by human leukaemia cells and slowed leukaemia progression in primary human acute-myeloid-leukaemia patient-derived xenografts. Model/species: Human leukaemia cell lines and primary human AML patient-derived xenografts Organism: Homo sapiens cells in mouse xenograft hosts Tissue/system: Leukaemic blasts Exposure: Pharmacological vitamin C Duration: Colony assays and xenograft progression Limits: Pharmacological vitamin C in a xenograft is not dietary intake, and a xenograft host lacks an intact immune system. Primary reference: [cimmino-2017] Restoration of TET2 function blocks aberrant self-renewal and leukemia progression (2017). https://pubmed.ncbi.nlm.nih.gov/28823558/ DOI: 10.1016/j.cell.2017.07.032
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.