{
  "abstract": "BRG1/BRM-associated factor (BAF) complexes are essential regulators of chromatin organization and cell identity. Genes encoding BAF subunits are among the most frequently mutated in human cancer. Yet, how disruption of a single subunit gives rise to distinct tumor states remains poorly understood. Atypical teratoid rhabdoid tumors (ATRTs) provide a compelling model, as they are uniformly driven by bi-allelic loss of the BAF subunit SMARCB1, yet segregate into distinct molecular subtypes. Using integrated multi-omics profiling of patient-derived ATRT organoids and primary tumor tissues, we show that transcriptional and chromatin accessibility changes upon SMARCB1 reconstitution are directed by subtype- and lineage-specific transcription factor (TF) repertoires. Genome-wide binding and transcriptomic analyses reveal that SMARCB1 reconstitution enables the lineage-specific TF RFX4 to engage regulatory elements and activate neuronal differentiation programs, partially reprogramming ATRT-MYC toward an ATRT-SHH-like identity. Together, these findings demonstrate that SMARCB1 loss disrupts TF-dependent chromatin priming, revealing that the lineage-specific regulatory output of BAF complexes is constrained by the underlying TF repertoire.",
  "abstract_shown": true,
  "affiliations": [
    "Princess Maxima Center for Pediatric Oncology"
  ],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 10,
  "authors": [
    {
      "name": "J. He"
    },
    {
      "name": "C. Rios Arceo"
    },
    {
      "name": "N. Anderson"
    },
    {
      "name": "W. Teunissen"
    },
    {
      "name": "I. Paassen"
    },
    {
      "name": "S. Jongsma"
    },
    {
      "name": "E. de Wit"
    },
    {
      "name": "M. Kool"
    },
    {
      "name": "N. Q. Liu"
    },
    {
      "affs": [
        0
      ],
      "name": "J. Drost"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/ev9364y553zh7.bib",
  "cited_by": 0,
  "doi": "10.64898/2026.11.08.764927",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.11.08.764927v1.full",
  "id": "ev9364y553zh7",
  "issns": [],
  "landing_url": "https://www.biorxiv.org/content/10.64898/2026.11.08.764927v1",
  "language": null,
  "licence": "CC-BY-NC-ND",
  "licence_label": "CC BY-NC-ND",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nc-nd/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "biorxiv",
      "cancer biology"
    ]
  ],
  "openalex": null,
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.11.08.764927v1.full.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-11-08",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/ev9364y553zh7.ris",
  "sources": [
    {
      "first_seen": "2026-11-11T12:23:39Z",
      "native_id": "10.64898/2026.11.08.764927",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.11.08.764927v1"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "biorxiv:cancer biology",
      "subfield": "oncology"
    }
  ],
  "title": "BAF complexes cooperate with lineage-restricted transcription factors to establish cell-state-specific regulatory programs",
  "title_text": "BAF complexes cooperate with lineage-restricted transcription factors to establish cell-state-specific regulatory programs",
  "type": "preprint",
  "updated_at": "2026-11-13T00:21:26Z",
  "url": "https://research.draconitic.com/paper/ev9364y553zh7",
  "venue": "bioRxiv",
  "versions": []
}