ArticleNature chemical biology2026
Mutant p53 protein accumulation is selectively targetable by proximity-inducing drugs.
Article in Nature chemical biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed.
- A Versatile DNA-Encoded Library Platform for the Discovery of Highly Cooperative Chemical Inducers of Proximity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Opportunities in cancer gene therapy: inhibiting MDM2 and restoring p14ARF as a means to activate p53.Molecular and cellular biochemistry · 2026Review
- Chemical Biology 2025: Highlights From the Ch/Bi145 Course at Caltech.Chembiochem : a European journal of chemical biology · 2026Review
- Harnessing p53 for Proximity Killing.International journal of molecular sciences · 2026Review
- Fuzuloparib enhances radiosensitivity of gain-of-function mutant p53 R273H NSCLC by promoting SLC7A11/GSH/GPX4 axis mediated ferroptosis.NPJ precision oncology · 2026Article
- Apoptosis signaling and cancer targeted therapy: from bench to bespoke.Translational cancer research · 2026Review
- Activating p53Nature communications · 2026Article
- Rewiring Oncogenic Transcriptional Complexes with Domain-ALTeration Chimeras (DALTACs) in Prostate Cancer.bioRxiv : the preprint server for biology · 2026Article
- An epigenetic bifunctional that toggles between transactivation and repression.bioRxiv : the preprint server for biology · 2026Article
- Targeting the p53 cancer mutants Y220C, Y220N, and Y220S with the small-molecule stabilizer rezatapopt.Cell death & disease · 2026Article
- Exploiting intracellular oncogenic proteins to release cytotoxins.RSC medicinal chemistry · 2026Article
- p53 Pathway-Targeted Therapeutic Strategies in Glioblastoma: A CNS-Specific Framework Integrating Therapeutic Resistance, Molecular Stratification, CNS Pharmacology, and Clinical Translation.Drug design, development and therapy · 2026Review
- Discovery of Non-Degradative Covalent Molecular Glues for Transcriptional Reprogramming.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
Abstract
TP53 mutant cancers are associated with approximately half of cancer deaths. The most common mechanism of p53 inactivation involves missense mutations. Such mutations in TP53 result in a robust upregulation of the p53 protein. Here, we demonstrate an induced proximity approach to selectively kill TP53 mutant cells. This approach uses the increased abundance of p53 protein in TP53 mutant cancer cells to concentrate toxic molecules in these cells. We demonstrate this approach with a molecule that binds the Y220C mutant of p53 and concentrates a PLK1 inhibitor in cells harboring TP53
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.