Component
Primary tumor growth in the SLC25A39 breast-cancer study
Primary tumor growth in the SLC25A39 breast-cancer study. Species, exposure and limitations are retained in each linked claim.
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
Primary tumor growth was unaffected by A39 loss in the reported comparison.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/glutathione-research/40736010.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e", "start_char": 0, "end_char": 1513, "text_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e"}
- experimental_model
- Genetic screens, cancer models and patient-derived xenografts
- exposure
- SLC25A39 loss and ATF4 CRISPR activation
- limitations
- Cancer-specific mechanism; no inference that dietary or supplemental GSH causes metastasis in people.
- nutrient_topic
- Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
- organism
- Experimental breast-cancer cells and mouse xenografts
- plain_language
- Early colonization and growth of the original tumor were distinct endpoints.
- primary_references
- [glutathione-p40736010] Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling. (2025). https://pubmed.ncbi.nlm.nih.gov/40736010/ DOI: 10.1158/2159-8290.cd-24-1556
- tissue_or_cell_type
- Early lung metastatic colonization
Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 1334–1345
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic screens, cancer models and patient-derived xenografts · source_derived_draft · unverified_draft
### glutathione-primary-tumor-null Primary tumor growth was unaffected by A39 loss in the reported comparison. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Early colonization and growth of the original tumor were distinct endpoints. organism: Experimental breast-cancer cells and mouse xenografts tissue_or_cell_type: Early lung metastatic colonization experimental_model: Genetic screens, cancer models and patient-derived xenografts limitations: Cancer-specific mechanism; no inference that dietary or supplemental GSH causes metastasis in people. exposure: SLC25A39 loss and ATF4 CRISPR activation evidence_span: {"source_cache": "artifacts/glutathione-research/40736010.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e", "start_char": 0, "end_char": 1513, "text_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e"} [glutathione-p40736010] Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling. (2025). https://pubmed.ncbi.nlm.nih.gov/40736010/ DOI: 10.1158/2159-8290.cd-24-1556
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.