{
  "abstract": "The mitotic chromosome periphery (MCP) is an important chromosome compartment but links to disease remains elusive. Here we define the mitosis-specific, Ki-67 interactome, identifying additional MCP components and revealing that MCP genes are commonly mutated in cancer, including nucleophosmin (NPM1). Acute myeloid leukaemia (AML)-specific NPM1 mutations (NPM1c + ), result in protein mislocalisation (nucleolus to cytoplasm). We demonstrate that NPM1c+ fails to adequately bind to the MCP, instead forming aggregates during mitosis. We also report that, de-compartmentalisation at mitotic onset allows formation of NPM1wt/c+ multimers. These mislocalisation mechanisms contribute to a significant hinderance of NPM1 re-entry into daughter cell nucleoli. Enhancing MCP loading capacity via Ki-67 overexpression resulted in increased MCP-bound NPM1c+ during mitosis and greater yield of nucleolar NPM1c + . Ki-67 expression demonstrated a significant interaction with NPM1 mutation status on AML patient overall survival, whereby higher Ki-67 was associated with increased hazard in NPM1wt but reduced hazard in NPM1c+ patients. This work reveals mechanistic insight into AML and evidence that the MCP has untapped therapeutic potential.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": null,
  "arxiv": null,
  "author_total": 9,
  "authors": [
    {
      "name": "Martin Grundy"
    },
    {
      "name": "Peter Woodmancy"
    },
    {
      "name": "Kellie Lucken"
    },
    {
      "name": "Xiaomeng Xing"
    },
    {
      "name": "Robert Markus",
      "orcid": "0000-0003-4535-303X"
    },
    {
      "name": "Seema Bagia"
    },
    {
      "name": "Sarah Storr",
      "orcid": "0000-0002-4103-6048"
    },
    {
      "name": "Claire H. Seedhouse",
      "orcid": "0000-0003-2280-4045"
    },
    {
      "name": "Daniel G. Booth",
      "orcid": "0000-0001-6216-2863"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/3y59ykwk4zmh2.bib",
  "cited_by": 0,
  "doi": "10.1038/s41467-026-78560-3",
  "fulltext_url": null,
  "id": "3y59ykwk4zmh2",
  "issns": [
    "2041-1723"
  ],
  "landing_url": "https://www.nature.com/articles/s41467-026-78560-3",
  "language": null,
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0",
  "metadata_licence": null,
  "native_subjects": [
    [
      "openalex",
      "2720|Acute Myeloid Leukemia Research"
    ]
  ],
  "openalex": "W7221555410",
  "pdf_url": "https://www.nature.com/articles/s41467-026-78560-3_reference.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-10-12",
  "publisher": "Springer Science and Business Media LLC",
  "ris": "https://research.draconitic.com/paper/3y59ykwk4zmh2.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:38Z",
      "native_id": "10.1038/s41467-026-78560-3",
      "source": "crossref",
      "url": "https://www.nature.com/articles/s41467-026-78560-3"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:2720|Acute Myeloid Leukemia Research",
      "subfield": "general"
    }
  ],
  "title": "Ki-67, the chromosome periphery and de-compartmentalisation each contribute to nucleophosmin mislocalisation in acute myeloid leukaemia",
  "title_text": "Ki-67, the chromosome periphery and de-compartmentalisation each contribute to nucleophosmin mislocalisation in acute myeloid leukaemia",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:17:38Z",
  "url": "https://research.draconitic.com/paper/3y59ykwk4zmh2",
  "venue": "Nature Communications",
  "versions": []
}