{
  "annotation_id": "b99e7a12-a835-4d44-a89b-31d74c08b0d9",
  "date_created": "2026-03-02T18:01:32.233000Z",
  "date_modified": "2026-03-02T18:01:32.233000Z",
  "file_hash": "8dd9ed6ed2b3292e01634496917f5beaf984a0e5a8d0c5db14e9366cfd4f3b44",
  "private": false,
  "record": {
    "abstract": "A new approach to the modular, complex systems analysis of nonlinear dynamics\nin cell cycling network transformations involved in carcinogenesis is proposed.\nCarcinogenesis is a complex process that involves dynamically inter-connected\nbiomolecules in the intercellular, membrane, cytosolic, nuclear and nucleolar\ncompartments that form numerous inter-related pathways. One such family of\npathways contains the cell cyclins. Cyclins are proteins that link several\ncritical pro-apoptotic and other cell cycling/division components, including\nthe tumor suppressor gene TP53 and its product, the Thomsen-Friedenreich\nantigen (T antigen), Rb, mdm2, c-Myc, p21, p27, Bax, Bad and Bcl-2, which all\nplay major roles in neoplastic transformation of many tissues. This novel\ntheoretical analysis based on recently published studies of cyclin signaling,\nwith special emphasis placed on the roles of cyclins D1 and E, suggests novel\nclinical trials and rational therapies of cancer through reestablishment of\ncell cycling inhibition in metastatic cancer cells.",
    "arxiv_id": "q-bio/0406046",
    "authors": [
      "V. I. Prisecaru",
      "I. C. Baianu"
    ],
    "categories": [
      "q-bio.MN"
    ],
    "title": "Cell Cycling Models of Carcinogenesis: A Complex Systems Analysis",
    "url": "https://arxiv.org/abs/q-bio/0406046"
  },
  "schema_id": "dorsal/arxiv",
  "source": {
    "execution_id": "0ab6cc3f-e26b-4dd0-8a3b-02779d9115c7",
    "id": "arXiv Dataset IDs",
    "type": "Model",
    "variant": "snapshot-2026-03-01",
    "version": "0.1.0"
  },
  "user_id": 1000002
}