Component

Patient-derived human AML cell growth in taurine experiments

Context-specific entity; species, compartment and exposure are stated on each claim.

2 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.

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.

Recorded relationships

What acts on it

  1. TAUT inhibition combined with venetoclax synergistically reduced growth of primary human AML cells in the reported experiments.

    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Ex-vivo human AML; venetoclax-resistance expression analyses.
    limitations
    Measured experimental combination effect, not a proven clinical interaction between taurine supplements and venetoclax.
    nutrient_topic
    Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
    plain_language
    Blocking nutrient uptake affected response to an anticancer drug in patient-derived cells.
    primary_references
    Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7

    Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 561–567

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Ex-vivo human AML; venetoclax-resistance expression analyses. · source_derived_draft · unverified_draft

    ## taurine-leukemia-venetoclax Blocking nutrient uptake affected response to an anticancer drug in patient-derived cells. TAUT inhibition combined with venetoclax synergistically reduced growth of primary human AML cells in the reported experiments. Model: Ex-vivo human AML; venetoclax-resistance expression analyses. Limitations: Measured experimental combination effect, not a proven clinical interaction between taurine supplements and venetoclax. Evidence access: Primary abstract Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
    Complete structured claim and evidence
  2. Inhibiting CDO1 in osteolineage cultures derived from AML patients reduced survival and colony formation of AML cells from the same patients.

    Experimental context and source evidence
    evidence_access
    Primary full text, Figure 2h–i
    experimental_model
    Matched human stromal/AML cocultures.
    limitations
    Ex-vivo dependency does not establish an effective or safe clinical inhibitor.
    nutrient_topic
    Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
    plain_language
    Patient-derived support cells also provided a growth-supporting pathway.
    primary_references
    Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7

    Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 521–527

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Matched human stromal/AML cocultures. · source_derived_draft · unverified_draft

    ## taurine-niche-human-cdo1 Patient-derived support cells also provided a growth-supporting pathway. Inhibiting CDO1 in osteolineage cultures derived from AML patients reduced survival and colony formation of AML cells from the same patients. Model: Matched human stromal/AML cocultures. Limitations: Ex-vivo dependency does not establish an effective or safe clinical inhibitor. Evidence access: Primary full text, Figure 2h–i Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards