{
 "meta": {
  "api_version": "1.0.0",
  "dataset_version": "2.0.1",
  "corpus_snapshot": "2026-10-12T22:59:14+0200",
  "source_commit": "93739c9d195dc39e47eecfabc3cab2565a2f256f",
  "license": "CC-BY-4.0",
  "cite": "Barton O. Oliver's mTOR Atlas. doi:10.5281/zenodo.22059963",
  "docs": "https://mtor-atlas.org/api/"
 },
 "data": {
  "id": "MTORC1-TUMOR",
  "claim": "mTORC1 activates Tumor growth",
  "source": {
   "name": "mTORC1",
   "entity": "mtorc1"
  },
  "target": {
   "name": "Tumor growth",
   "entity": "tumor-growth"
  },
  "effect": "activates",
  "type": "functional-consequence",
  "directness": "indirect",
  "timescale": "chronic",
  "compartment": null,
  "map_band": "outcome",
  "species": [
   "mouse",
   "human cells"
  ],
  "mechanism": "Hyperactive mTORC1 reprograms translation toward a specific set of pro-growth and pro-metastasis mRNAs (HSI2012, prostate models) and couples nucleotide synthesis to demand, creating a targetable vulnerability in TSC-deficient cells (VAL2017).",
  "mechanism_beginner": "In mouse tumour models and cancer cells where the pathway is already over-active, hyperactive mTORC1 pushes cells to build a specific set of growth- and spread-promoting proteins, and the tumour becomes dependent on that programme.",
  "context": null,
  "boundary": "Context-dependent: shown in genetically driven mouse tumour models and cancer cell lines with hyperactive mTORC1 (PTEN loss, TSC loss), not as a general property of tumours. OKI2021 (mouse AML) is not cited as support: mTORC1 activity fell as the leukaemia progressed and rose during the chemotherapy response, so it bears on when to inhibit mTORC1, not on mTORC1 driving growth.",
  "note": "The arrow means hyperactive mTORC1 promotes tumour growth where the pathway is already unleashed - PTEN-loss and TSC-loss backgrounds. It is not a claim that mTORC1 activity causes tumours generally, and normal mTORC1 signalling is not a tumour driver here.",
  "consensus_contested": false,
  "curation_contested": false,
  "contested": false,
  "confidence": {
   "mechanistic": "high",
   "human_relevance": "plausible",
   "consensus": "established"
  },
  "evidence": {
   "kind": "Genetic epistasis",
   "strongest": {
    "code": "A",
    "label": "Animal model"
   },
   "supporting": [
    "HSI2010",
    "HSI2012",
    "VAL2017",
    "INO2006",
    "FER2026"
   ],
   "conflicting": []
  },
  "external_refs": [],
  "reviewed": null,
  "updated": null,
  "checked": null,
  "review_status": "unreviewed",
  "reviewer": null,
  "curation_status": "Proposed",
  "url": "https://mtor-atlas.org/relation/MTORC1-TUMOR/",
  "api_url": "https://mtor-atlas.org/api/v1/relations/MTORC1-TUMOR.json"
 }
}