{
  "abstract": "TP53 mutations create two functionally opposite states—loss of the protein or retention of a full-length mutant protein—yet are usually reported as one entity. How the two states are distributed between solid tumors and hematologic malignancies has not been quantified. In one pipeline integrating ≈64,000 samples (29 solid-tumor types, 19 hematologic cohorts and a 42,714-sample post-therapy clonal-hematopoiesis cohort), we asked which state is selected where, what it does, and what it offers. Truncating mutations accounted for 34.2% of solid but 24.4% of hematologic alterations (χ2 = 33.7, p = 2.3 × 10−7; reproduced in the NCI TP53 and COSMIC databases). Where copy number resolves allelic state, 60.6% of missense-mutant solid tumors had lost the wild-type allele (19.5% biallelic inactivation). Blood retained full-length missense protein instead, and in MDS, outcome tracked the retained-allele dose (hazard ratio 1.78, p = 1.0 × 10−4); in solid tumors, no survival difference was detected by allelic state. The endogenous CpG baseline is equivalent (20.7% versus 21.2%), while solid spectra carry exogenous exposure fingerprints. Only the retained state presents a target, so allele-specific reactivation is the rational corollary where retention prevails—a hypothesis, as retention in blood is inferred from mutation class.",
  "abstract_shown": true,
  "affiliations": [
    "Department of Hematologic Oncology, Guangxi Medical University Cancer Hospital, Nanning 530200, China"
  ],
  "article_type": null,
  "arxiv": null,
  "author_total": 5,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Haichun Huang"
    },
    {
      "affs": [
        0
      ],
      "name": "Yikui Xie",
      "orcid": "0009-0000-8884-5750"
    },
    {
      "affs": [
        0
      ],
      "name": "Baoping Guo"
    },
    {
      "affs": [
        0
      ],
      "name": "Ying Duan"
    },
    {
      "affs": [
        0
      ],
      "name": "Hong Cen"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/6zcmb36zvvk4p.bib",
  "cited_by": 0,
  "doi": "10.3390/ijms272110024",
  "fulltext_url": null,
  "id": "6zcmb36zvvk4p",
  "issns": [
    "1422-0067"
  ],
  "landing_url": "https://www.mdpi.com/1422-0067/27/21/10024",
  "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": "2026-11-09",
  "publisher": "MDPI AG",
  "ris": "https://research.draconitic.com/paper/6zcmb36zvvk4p.ris",
  "sources": [
    {
      "first_seen": "2026-11-09T12:22:39Z",
      "native_id": "10.3390/ijms272110024",
      "source": "crossref",
      "url": "https://www.mdpi.com/1422-0067/27/21/10024"
    }
  ],
  "subjects": [
    {
      "field": "biochemistry",
      "origin": "issn:1422-0067",
      "subfield": "general"
    }
  ],
  "title": "One Gene, Two States: Truncating Loss Versus Retained Full-Length p53 in Solid and Hematologic Cancers",
  "title_text": "One Gene, Two States: Truncating Loss Versus Retained Full-Length p53 in Solid and Hematologic Cancers",
  "type": "peer-reviewed",
  "updated_at": "2026-11-10T00:21:27Z",
  "url": "https://research.draconitic.com/paper/6zcmb36zvvk4p",
  "venue": "International Journal of Molecular Sciences",
  "versions": []
}