{
  "abstract": "Hormone-driven cancers, including prostate, breast, endometrial and ovarian cancers, are a leading cause of cancer-related mortality. Endocrine therapies targeting androgen receptor and oestrogen receptor/progesterone receptor signalling have improved outcomes, but acquired resistance arising through genetic and epigenetic mechanisms that bypass receptor dependence remains a major challenge. BORIS (Brother of the Regulator of Imprinted Sites), a CTCF paralogue, is a germline-restricted regulator that becomes aberrantly reactivated in cancer through promoter hypomethylation, p53 loss, and loss of CTCF-mediated repression. Once expressed, BORIS occupies CTCF sites, displacing or co-occupying them with CTCF, and reprograms clustered sites into alternative transcriptional start sites through SRCAP-mediated H2A.Z deposition, activating germline genes that sustain proliferation, and therapeutic resistance. BORIS expression correlates with poor prognosis in ovarian and endometrial cancers, associates with ER/PR levels in breast cancer, and correlates with Gleason score in prostate cancer. BORIS represses AR signalling in ovarian cancer and inversely correlates with receptor expression in endometrial cancer. Its cancer-testis antigen properties position BORIS as an immunotherapy target, with preclinical vaccine efficacy demonstrated in breast cancer models. This review synthesises the disease-specific evidence positioning BORIS as a driver of transcriptional reprogramming and endocrine resistance, identifies current knowledge gaps, and discusses translational implications of targeting this pathway.",
  "abstract_shown": true,
  "affiliations": [
    "Newcastle University Centre for Cancer, Paul O’Gorman Building, Newcastle upon Tyne NE2 4AD, UK",
    "Faculty of Biomedical Sciences, University of Benghazi, Benghazi P.O. Box 1308, Libya"
  ],
  "article_type": null,
  "arxiv": null,
  "author_total": 3,
  "authors": [
    {
      "affs": [
        0,
        1
      ],
      "name": "Sara Saleem",
      "orcid": "0009-0009-2524-5657"
    },
    {
      "affs": [
        0
      ],
      "name": "Luke Gaughan"
    },
    {
      "affs": [
        0
      ],
      "name": "Craig N. Robson",
      "orcid": "0000-0002-9628-6669"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/6tbn4fyrg4ecm.bib",
  "cited_by": 0,
  "doi": "10.3390/cells15212001",
  "fulltext_url": null,
  "id": "6tbn4fyrg4ecm",
  "issns": [
    "2073-4409"
  ],
  "landing_url": "https://www.mdpi.com/2073-4409/15/21/2001",
  "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": null,
  "pdf_url": null,
  "pmcid": null,
  "pmid": null,
  "published": "2026-11-03",
  "publisher": "MDPI AG",
  "ris": "https://research.draconitic.com/paper/6tbn4fyrg4ecm.ris",
  "sources": [
    {
      "first_seen": "2026-11-03T12:21:14Z",
      "native_id": "10.3390/cells15212001",
      "source": "crossref",
      "url": "https://www.mdpi.com/2073-4409/15/21/2001"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "issn:2073-4409",
      "subfield": "cell-biology"
    }
  ],
  "title": "BORIS in Hormone-Driven Cancers: Epigenetic Reprogramming, Transcriptional Plasticity, and Therapeutic Implications",
  "title_text": "BORIS in Hormone-Driven Cancers: Epigenetic Reprogramming, Transcriptional Plasticity, and Therapeutic Implications",
  "type": "peer-reviewed",
  "updated_at": "2026-11-05T00:20:59Z",
  "url": "https://research.draconitic.com/paper/6tbn4fyrg4ecm",
  "venue": "Cells",
  "versions": []
}