Component
FGFR1 cysteine/methionine oxidation in the 2026 osteosarcoma study
FGFR1 cysteine/methionine oxidation in the 2026 osteosarcoma study. Species, exposure and limitations are retained in each linked 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.
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 it acts on
FGFR1 oxidation promoted receptor activation and downstream signaling in the phosphate-sensing tumor-model experiments.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/phosphorus-research/42247296.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76", "start_char": 0, "end_char": 1041, "text_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76"}
- experimental_model
- Osteosarcoma-cell signaling with in-vivo tumor experiments
- exposure
- Elevated phosphate challenges and receptor activation experiments
- limitations
- New 2026 mechanism in tumor models; blood-Pi/tumor-growth association is not proof that dietary phosphorus causes human cancer. No specific transporter or oxidized residue number is invented from the abstract.
- nutrient_topic
- Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
- organism
- Osteosarcoma cellular and animal systems; precise species not fully resolved from abstract
- plain_language
- Phosphate triggered receptor signaling through an indirect chemical route.
- primary_references
- [phosphorus-p42247296] Unconventional activation of the proto-oncogene FGFR1 by extracellular phosphate via H2O2-mediated kinase oxidation. (2026). https://pubmed.ncbi.nlm.nih.gov/42247296/ DOI: 10.1016/j.celrep.2026.117504
- tissue_or_cell_type
- Plasma-membrane/mitochondrial phosphate handling and FGFR1 signaling
Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 893–904
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Osteosarcoma-cell signaling with in-vivo tumor experiments · source_derived_draft · unverified_draft
### phosphorus-fgfr-activation FGFR1 oxidation promoted receptor activation and downstream signaling in the phosphate-sensing tumor-model experiments. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: Phosphate triggered receptor signaling through an indirect chemical route. organism: Osteosarcoma cellular and animal systems; precise species not fully resolved from abstract tissue_or_cell_type: Plasma-membrane/mitochondrial phosphate handling and FGFR1 signaling experimental_model: Osteosarcoma-cell signaling with in-vivo tumor experiments limitations: New 2026 mechanism in tumor models; blood-Pi/tumor-growth association is not proof that dietary phosphorus causes human cancer. No specific transporter or oxidized residue number is invented from the abstract. exposure: Elevated phosphate challenges and receptor activation experiments evidence_span: {"source_cache": "artifacts/phosphorus-research/42247296.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76", "start_char": 0, "end_char": 1041, "text_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76"} [phosphorus-p42247296] Unconventional activation of the proto-oncogene FGFR1 by extracellular phosphate via H2O2-mediated kinase oxidation. (2026). https://pubmed.ncbi.nlm.nih.gov/42247296/ DOI: 10.1016/j.celrep.2026.117504
Complete structured claim and evidence
What acts on it
The phosphate-associated hydrogen-peroxide burst oxidized critical cysteine and methionine residues of FGFR1.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/phosphorus-research/42247296.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76", "start_char": 0, "end_char": 1041, "text_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76"}
- experimental_model
- Osteosarcoma-cell signaling with in-vivo tumor experiments
- exposure
- Elevated phosphate challenges and receptor activation experiments
- limitations
- New 2026 mechanism in tumor models; blood-Pi/tumor-growth association is not proof that dietary phosphorus causes human cancer. No specific transporter or oxidized residue number is invented from the abstract.
- nutrient_topic
- Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
- organism
- Osteosarcoma cellular and animal systems; precise species not fully resolved from abstract
- plain_language
- A redox change reached the receptor protein.
- primary_references
- [phosphorus-p42247296] Unconventional activation of the proto-oncogene FGFR1 by extracellular phosphate via H2O2-mediated kinase oxidation. (2026). https://pubmed.ncbi.nlm.nih.gov/42247296/ DOI: 10.1016/j.celrep.2026.117504
- tissue_or_cell_type
- Plasma-membrane/mitochondrial phosphate handling and FGFR1 signaling
Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 880–891
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Osteosarcoma-cell signaling with in-vivo tumor experiments · source_derived_draft · unverified_draft
### phosphorus-peroxide-fgfr The phosphate-associated hydrogen-peroxide burst oxidized critical cysteine and methionine residues of FGFR1. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: A redox change reached the receptor protein. organism: Osteosarcoma cellular and animal systems; precise species not fully resolved from abstract tissue_or_cell_type: Plasma-membrane/mitochondrial phosphate handling and FGFR1 signaling experimental_model: Osteosarcoma-cell signaling with in-vivo tumor experiments limitations: New 2026 mechanism in tumor models; blood-Pi/tumor-growth association is not proof that dietary phosphorus causes human cancer. No specific transporter or oxidized residue number is invented from the abstract. exposure: Elevated phosphate challenges and receptor activation experiments evidence_span: {"source_cache": "artifacts/phosphorus-research/42247296.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76", "start_char": 0, "end_char": 1041, "text_sha256": "a8d4221d8a5c56a5937ab8262e3ece5ed87692cb876ddcc0a08e7f68b66a9b76"} [phosphorus-p42247296] Unconventional activation of the proto-oncogene FGFR1 by extracellular phosphate via H2O2-mediated kinase oxidation. (2026). https://pubmed.ncbi.nlm.nih.gov/42247296/ DOI: 10.1016/j.celrep.2026.117504
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
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Open hypotheses
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This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.