Component

Ferroptosis in human pancreatic cancer models

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

4 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. Adding CoA prevented ferroptosis induced by imidazole ketone erastin in the reported PDAC cell experiments.

    Coenzyme A → Ferroptosis in human pancreatic cancer models source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human PDAC culture and exogenous CoA treatment.
    limitations
    Cell-culture rescue does not establish oral CoA absorption, intact cellular uptake in vivo or clinical efficacy.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Restoring a downstream metabolite bypassed part of an upstream block in culture.
    primary_references
    Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 220–226

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human PDAC culture and exogenous CoA treatment. · source_derived_draft · unverified_draft

    ## l-cysteine-pdac-coa-rescue Restoring a downstream metabolite bypassed part of an upstream block in culture. Adding CoA prevented ferroptosis induced by imidazole ketone erastin in the reported PDAC cell experiments. Model: Human PDAC culture and exogenous CoA treatment. Limitations: Cell-culture rescue does not establish oral CoA absorption, intact cellular uptake in vivo or clinical efficacy. Evidence access: Primary full text Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872
    Complete structured claim and evidence

  2. Cystine starvation induced lipid oxidation and ferroptosis in four of five tested human PDAC cell lines.

    Cystine → Ferroptosis in human pancreatic cancer models source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human pancreatic cancer cultures; nutrient withdrawal, oxidation and viability assays.
    limitations
    Culture starvation is not dietary treatment; one of the tested lines differed.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Dependence on external sulfur varied between cancer-cell models.
    primary_references
    Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 180–186

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human pancreatic cancer cultures; nutrient withdrawal, oxidation and viability assays. · source_derived_draft · unverified_draft

    ## l-cysteine-pdac-cystine-withdrawal Dependence on external sulfur varied between cancer-cell models. Cystine starvation induced lipid oxidation and ferroptosis in four of five tested human PDAC cell lines. Model: Human pancreatic cancer cultures; nutrient withdrawal, oxidation and viability assays. Limitations: Culture starvation is not dietary treatment; one of the tested lines differed. Evidence access: Primary full text Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872
    Complete structured claim and evidence

  3. Pantothenate-kinase inhibition combined with BSO synergistically induced ferroptosis in the reported PDAC assays.

    Combined pantothenate-kinase and GSH-synthesis inhibition → Ferroptosis in human pancreatic cancer models source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human PDAC culture; pharmacological PANKi/BSO combination.
    limitations
    This is a demonstrated drug-combination interaction in this assay, not evidence for oral B5/cysteine supplement synergy.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Two protective branches were experimentally blocked together.
    primary_references
    Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 212–218

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human PDAC culture; pharmacological PANKi/BSO combination. · source_derived_draft · unverified_draft

    ## l-cysteine-pdac-dual-block Two protective branches were experimentally blocked together. Pantothenate-kinase inhibition combined with BSO synergistically induced ferroptosis in the reported PDAC assays. Model: Human PDAC culture; pharmacological PANKi/BSO combination. Limitations: This is a demonstrated drug-combination interaction in this assay, not evidence for oral B5/cysteine supplement synergy. Evidence access: Primary full text Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872
    Complete structured claim and evidence

  4. Buthionine sulfoximine lowered glutathione without inducing lipid oxidation or loss of viability under the tested PDAC conditions.

    GSH synthesis inhibition with BSO in PDAC cells → Ferroptosis in human pancreatic cancer models source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human PDAC cultures, BSO and viability/lipid-ROS assays.
    limitations
    This null result is model-specific; it does not make glutathione dispensable in general.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Loss of glutathione alone did not explain the whole cysteine-depletion effect.
    primary_references
    Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 204–210

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human PDAC cultures, BSO and viability/lipid-ROS assays. · source_derived_draft · unverified_draft

    ## l-cysteine-pdac-gsh-only-limit Loss of glutathione alone did not explain the whole cysteine-depletion effect. Buthionine sulfoximine lowered glutathione without inducing lipid oxidation or loss of viability under the tested PDAC conditions. Model: Human PDAC cultures, BSO and viability/lipid-ROS assays. Limitations: This null result is model-specific; it does not make glutathione dispensable in general. Evidence access: Primary full text Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872
    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