{
 "meta": {
  "api_version": "1.0.0",
  "dataset_version": "2.0.1+unreleased",
  "live_matches_release": false,
  "archived_release": {
   "version": "2.0.1",
   "version_doi": "10.5281/zenodo.23090261",
   "date": "2026-10-01",
   "studies": 428
  },
  "data_fingerprint": "21bd609b55973b7b5b84e545fdde629d79115243854f1595680c534e6e1ef96f",
  "corpus_snapshot": "2026-11-02T19:05:06+0100",
  "source_commit": "1e9de0d56d4ea503818c4095460addc4a0c7f4a3",
  "license": "CC-BY-4.0",
  "cite": "Barton O. Oliver's mTOR Atlas (live data, not an archived version; give corpus_snapshot and source_commit). doi:10.5281/zenodo.22059963",
  "docs": "https://mtor-atlas.org/api/"
 },
 "data": {
  "id": "MTORC1-RCC",
  "claim": "mTORC1 is associated with Renal cell carcinoma (RCC)",
  "source": {
   "name": "mTORC1",
   "entity": "mtorc1"
  },
  "target": {
   "name": "Renal cell carcinoma (RCC)",
   "entity": "renal-cell-carcinoma-rcc"
  },
  "effect": "associated-with",
  "type": "association",
  "directness": "unresolved",
  "timescale": "chronic",
  "compartment": null,
  "map_band": "outcome",
  "species": [
   "human"
  ],
  "mechanism": "Renal cancers frequently carry lesions that leave mTORC1 constitutively active, which is why this tissue responds to mTOR inhibitors. In two phase III trials in metastatic RCC, temsirolimus extended overall survival versus interferon alfa in poor-prognosis patients (HUD2007), and everolimus extended progression-free survival versus placebo after VEGF-targeted therapy (MOT2008). That the tumour responds to the drug is not the same as mTORC1 initiating the cancer.",
  "mechanism_beginner": "Many kidney cancers carry changes that leave mTORC1 stuck \"on\", which is why this cancer responds to mTOR-blocking drugs at all. In one large trial, people with advanced kidney cancer lived longer on temsirolimus; in another, everolimus slowed the cancer's growth for a few months. Responding to the drug is not proof that mTORC1 started the cancer.",
  "context": null,
  "boundary": "Correlative, plus two randomised human trials showing the tumour responds to mTOR inhibitors: overall survival in poor-prognosis first-line RCC with temsirolimus (HUD2007), progression-free survival only after VEGF-targeted therapy with everolimus (MOT2008). This is response to treatment, not a demonstration that mTORC1 activation initiates RCC. The bladder-cancer responder case IYE2012 was removed from this edge on 2026-10-09 as a citation-population mismatch (it describes bladder, not kidney).",
  "boundary_tags": [],
  "conflict": null,
  "note": "Replaces TUMOR-RCC, which asserted 'Tumor growth activates RCC' - a category error, since RCC is an instance of tumour growth, not a downstream target. 2026-10-09: IYE2012 (metastatic bladder cancer) removed as a supporting study and from the mechanism text; it was a citation-population mismatch. Human relevance now rests on the two RCC phase III trials MOT2008 and HUD2007. 2026-10-09 (later): corrected 'both trials extended survival' - only HUD2007 showed overall survival; MOT2008 (RECORD-1) showed progression-free survival. 2026-10-10: this record is typed as an association, but the published data still carried the causal sign 'activates', and several surfaces built their wording from that sign rather than from the type. A first attempt the same day fixed the API claim string and the relation-page heading, and this note then claimed the problem was solved. It was not: the static pathway table, the link labels on both supporting study pages, four Practice Arena questions and the arrowhead on the map all still read causally. 2026-10-10 (second pass): fixed in the data instead of in one renderer. The published effect for a non-causal relation type is now 'associated-with' with causal=false, and the curatorial Airtable sign is kept separately as sign_curatorial, so every surface follows from one value. The map draws an open circle rather than an arrowhead. A new build gate fails if a non-causal type ever carries a causal sign again. What this edge does and does not claim: lesions in the pathway are frequent in renal cell carcinoma and mTOR inhibitors benefit defined patient populations, but no study here establishes that mTORC1 activity drives the disease. Whether to split the record into a molecular mechanism plus a separate clinical-outcome record is an open editorial question.",
  "consensus_contested": false,
  "curation_contested": false,
  "contested": false,
  "confidence": {
   "mechanistic": "low",
   "human_relevance": "established",
   "consensus": "emerging"
  },
  "evidence": {
   "kind": "Correlative",
   "strongest": {
    "code": "H",
    "label": "Human study"
   },
   "supporting": [
    "MOT2008",
    "HUD2007"
   ],
   "conflicting": []
  },
  "external_refs": [],
  "reviewed": null,
  "updated": null,
  "checked": null,
  "review_status": "unreviewed",
  "reviewer": null,
  "curation_status": "Proposed",
  "url": "https://mtor-atlas.org/relation/MTORC1-RCC/",
  "api_url": "https://mtor-atlas.org/api/v1/relations/MTORC1-RCC.json"
 }
}