Component

Human cancer-cell survival with DNA-damaging treatment

Human cancer-cell survival with DNA-damaging treatment

2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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. ALCAR reversed increased sensitivity to DNA-damaging agents caused by disruption of the alpha-ketoglutarate–carnitine axis.

    Acetyl-L-carnitine → Human cancer-cell survival with DNA-damaging treatment Recorded from sourceungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_model
    Human HR-proficient CCNE1 cancer-cell models; Results and supplementary Fig. 3.
    interpretation_status
    Source-derived curation with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Acetyl-L-carnitine collection; exact intervention and molecular form govern interpretation. · Acetyl-L-carnitine
    plain_language
    ALCAR reversed increased sensitivity to DNA-damaging agents caused by disruption of the alpha-ketoglutarate–carnitine axis.
    primary_references
    αKG-mediated carnitine synthesis drives DNA repair via histone acetylation. | https://pubmed.ncbi.nlm.nih.gov/42203879/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13307467/ | https://doi.org/10.1038/s41586-026-10584-7
    source_locator
    Reviewed reference cancer-drug-rescue; The study tested distinct upstream restrictions including IDH1 inhibition, glutamine starvation and TMLHE knockdown. Propionylcarnitine and butyrylcarnitine did not reproduce this rescue. This is a context-qualified summary of rescue contrasts, not an isolated basal ALCAR effect.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 336–342

    AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · Human HR-proficient CCNE1 cancer-cell models; Results and supplementary Fig. 3. · Recorded from source · Recorded from source

    ### cancer-drug-rescue ALCAR reversed increased sensitivity to DNA-damaging agents caused by disruption of the alpha-ketoglutarate–carnitine axis. The study tested distinct upstream restrictions including IDH1 inhibition, glutamine starvation and TMLHE knockdown. Propionylcarnitine and butyrylcarnitine did not reproduce this rescue. This is a context-qualified summary of rescue contrasts, not an isolated basal ALCAR effect. Model and exposure: Human HR-proficient CCNE1 cancer-cell models; Results and supplementary Fig. 3. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: αKG-mediated carnitine synthesis drives DNA repair via histone acetylation. | 2026 | https://pubmed.ncbi.nlm.nih.gov/42203879/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13307467/ | https://doi.org/10.1038/s41586-026-10584-7 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    Complete structured claim and evidence

  2. ALCAR did not rescue DNA-damage sensitivity when histone acetyltransferase activity was inhibited.

    Acetyl-L-carnitine → Human cancer-cell survival with DNA-damaging treatment Recorded from sourceungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_contrast
    {"intervention": "ALCAR plus HAT inhibition and DNA-damaging treatment", "comparator": "Same HAT inhibition and DNA-damaging treatment without ALCAR", "endpoint": "ALCAR did not rescue DNA-damage sensitivity when histone acetyltransferase activity was inhibited.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    CCNE1-driven human cell models; HAT inhibition plus DNA-damaging agents; Extended Data Fig. 5.
    interpretation_status
    Source-derived curation with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Acetyl-L-carnitine collection; exact intervention and molecular form govern interpretation. · Acetyl-L-carnitine
    plain_language
    ALCAR did not rescue DNA-damage sensitivity when histone acetyltransferase activity was inhibited.
    primary_references
    αKG-mediated carnitine synthesis drives DNA repair via histone acetylation. | https://pubmed.ncbi.nlm.nih.gov/42203879/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13307467/ | https://doi.org/10.1038/s41586-026-10584-7
    source_locator
    Reviewed reference cancer-hat-no-rescue; Supplying substrate failed when downstream acetylation machinery was blocked. The tested HAT inhibitor and individual drug concentrations are not fully extracted here; no universal inhibitor equivalence is asserted.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 328–334

    AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · CCNE1-driven human cell models; HAT inhibition plus DNA-damaging agents; Extended Data Fig. 5. · Recorded from source · Recorded from source

    ### cancer-hat-no-rescue ALCAR did not rescue DNA-damage sensitivity when histone acetyltransferase activity was inhibited. Supplying substrate failed when downstream acetylation machinery was blocked. The tested HAT inhibitor and individual drug concentrations are not fully extracted here; no universal inhibitor equivalence is asserted. Model and exposure: CCNE1-driven human cell models; HAT inhibition plus DNA-damaging agents; Extended Data Fig. 5. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: αKG-mediated carnitine synthesis drives DNA repair via histone acetylation. | 2026 | https://pubmed.ncbi.nlm.nih.gov/42203879/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13307467/ | https://doi.org/10.1038/s41586-026-10584-7 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    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.