ArticleNature genetics2025
Deep CRISPR mutagenesis characterizes the functional diversity of TP53 mutations.
Article in Nature genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
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Who cites it
65 citing papers in PubMed.
- Probabilistic mapping of sub-genic intolerance reveals functional and disease-critical protein regions.bioRxiv : the preprint server for biology · 2026Article
- Large serine recombinase-mediated gene insertion for high-throughput screens: advantages, design principles, and applications.Nucleic acids research · 2026Review
- Variation at the R181 Residue of p53 Confers Loss of p53 DNA Binding Cooperativity with the Retention of Mitochondria-Associated Apoptosis.Molecular cancer research : MCR · 2026Article
- Reclassification ofCurrent oncology (Toronto, Ont.) · 2026Article
- Mutant TP53 hijacks RNA-splicing factor RBM28 to suppress double-stranded RNA triggered antitumor immunity.Nature communications · 2026Article
- Compound delivery of eVLPs enhances prime editing for targeted genome engineering and high-throughput screening.Cell genomics · 2026Article
- Secreted luciferases as a minimally invasive 3R-compliant tool for accurate monitoring of tumor burden.Nature protocols · 2026Review
- Tumor patterns and cancer risk in carriers of TP53 exonic germline variants that alter mRNA splicing.European journal of human genetics : EJHG · 2026Article
- Fragility of precision: resistance to mutant p53 reactivation.Signal transduction and targeted therapy · 2026Article
- Combining multiplexed functional data to improve variant classification.Genome medicine · 2026Article
- mTORC1 suppression by Trp53 mutation drives resistance to immune checkpoint blockade.Cell death & disease · 2026Article
- A Personalized Therapeutic Approach for Liver Cancers Expressing the African-Centric P47S Variant of TP53.Molecular cancer research : MCR · 2026Article
- Primer-walking sequencing identifies predominantly noncoding TP53 variants in canine cancers.Journal of veterinary science · 2026Article
- Single-cell analysis reveals an endothelial TP53-CXCL14 axis in breast cancer progression.Journal of translational medicine · 2026Article
- Effect of Algal Lectin Siye on Proliferation and Apoptosis of Breast and Colon Cancer Cells.Marine drugs · 2026Article
- Causal Prediction of TP53 Variant Pathogenicity Using a Perturbation-Informed Protein Language Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Genotypic and phenotypic characteristics of germline TP53 variant carriers: experience from two cancer genetic counseling units.Familial cancer · 2026Article
- Pancancer Fine-Mapping of Mutational Intolerance Identifies CHEK1 as an Immunosuppressive Driver in Lung Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Low-penetrance TP53 variants are mainly hypomorphic: an underestimated issue with high clinical significance.NPJ genomic medicine · 2026Article
- GDPD5-CD55-EGFR competitive binding axis regulates radioresistance and lipid accumulation in rectal cancer.Cell death & disease · 2026Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
25 authors.
Funding
Abstract
The mutational landscape of TP53, a tumor suppressor mutated in about half of all cancers, includes over 2,000 known missense mutations. To fully leverage TP53 mutation status for personalized medicine, a thorough understanding of the functional diversity of these mutations is essential. We conducted a deep mutational scan using saturation genome editing with CRISPR-mediated homology-directed repair to engineer 9,225 TP53 variants in cancer cells. This high-resolution approach, covering 94.5% of all cancer-associated TP53 missense mutations, precisely mapped the impact of individual mutations on tumor cell fitness, surpassing previous deep mutational scan studies in distinguishing benign from pathogenic variants. Our results revealed even subtle loss-of-function phenotypes and identified promising mutants for pharmacological reactivation. Moreover, we uncovered the roles of splicing alterations and nonsense-mediated messenger RNA decay in mutation-driven TP53 dysfunction. These findings underscore the power of saturation genome editing in advancing clinical TP53 variant interpretation for genetic counseling and personalized cancer therapy.
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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 Socratic graph.