Component

Apoptosis in specified EGCG cancer models

Study-scoped entity; inspect species, exposure, model and limitations on each claim.

3 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. Acid sphingomyelinase participated downstream of PKC delta in 67LR-dependent cell death.

    Acid sphingomyelinase family → Apoptosis in specified EGCG cancer models source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Cancer-cell experiments and mouse xenografts in the 2013 study.
    limitations
    Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    Lipid breakdown was part of the experimental death signal.
    primary_references
    67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 76–82

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cancer-cell experiments and mouse xenografts in the 2013 study. · source_derived_draft · unverified_draft

    ## egcg-asm Lipid breakdown was part of the experimental death signal. Acid sphingomyelinase participated downstream of PKC delta in 67LR-dependent cell death. Model: Cancer-cell experiments and mouse xenografts in the 2013 study. Limitations: Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety. Evidence access: primary abstract. 67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768
    Complete structured claim and evidence

  2. Overexpressed PDE5 attenuated the cGMP-dependent anticancer signal.

    Phosphodiesterase 5 family → Apoptosis in specified EGCG cancer models source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Cancer-cell experiments and mouse xenografts in the 2013 study.
    limitations
    Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    An enzyme that removes cGMP can limit the response.
    primary_references
    67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 84–90

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cancer-cell experiments and mouse xenografts in the 2013 study. · source_derived_draft · unverified_draft

    ## egcg-pde5 An enzyme that removes cGMP can limit the response. Overexpressed PDE5 attenuated the cGMP-dependent anticancer signal. Model: Cancer-cell experiments and mouse xenografts in the 2013 study. Limitations: Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety. Evidence access: primary abstract. 67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768
    Complete structured claim and evidence

  3. PDE5 inhibition with vardenafil potentiated EGCG-dependent apoptosis and prolonged survival in a mouse xenograft experiment.

    Vardenafil → Apoptosis in specified EGCG cancer models source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Cancer-cell experiments and mouse xenografts in the 2013 study.
    limitations
    Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    Blocking the opposing enzyme strengthened the response in these models.
    primary_references
    67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 92–98

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cancer-cell experiments and mouse xenografts in the 2013 study. · source_derived_draft · unverified_draft

    ## egcg-vardenafil Blocking the opposing enzyme strengthened the response in these models. PDE5 inhibition with vardenafil potentiated EGCG-dependent apoptosis and prolonged survival in a mouse xenograft experiment. Model: Cancer-cell experiments and mouse xenografts in the 2013 study. Limitations: Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety. Evidence access: primary abstract. 67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768
    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