ReviewCold Spring Harbor perspectives in medicine2016
Somatic TP53 Mutations in the Era of Genome Sequencing.
Review in Cold Spring Harbor perspectives in medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers, 1 of them a synthesis that pooled it.
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Who cites it
152 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023Pooled it
- Aflatoxin-associated hepatocarcinogenesis in a changing climate: the gut microbiome as a missing link in the One Health framework.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- p53 in Canine Mammary Tumors: From Molecular Pathogenesis to Biomarker Applications and Comparative Oncology.Veterinary sciences · 2026Review
- Tumor patterns and cancer risk in carriers of TP53 exonic germline variants that alter mRNA splicing.European journal of human genetics : EJHG · 2026Article
- Article
- MST4 plays dual roles in lung adenocarcinoma by regulating homeostasis of wild-type and mutant p53 protein.Oncogene · 2026Article
- Selective Elimination of TP53 Mutant Cells by Transcript-Activated Chromatin Shredding.bioRxiv : the preprint server for biology · 2026Article
- Article
- A catalogue of missense and nonsense mutation abundances for the U.S. cancer patient population.medRxiv : the preprint server for health sciences · 2026Article
- Low-penetrance TP53 variants are mainly hypomorphic: an underestimated issue with high clinical significance.NPJ genomic medicine · 2026Article
- Identification and characterization of BRAF⇔TP53 interactions in melanoma.Cell reports · 2026Article
- Fibroblast-associated CTHRC1 as a key indicator of recurrence risk in prostate cancer.World journal of surgical oncology · 2026Article
- Four Metachronous Cancers: Mutation Profiling Can Be Used to Distinguish Multiple Primary Cancers from Metastases.Internal medicine (Tokyo, Japan) · 2026Article
- Aflatoxin Mixture-Driven Intrahepatic Cholangiocarcinoma in Rats Involving G1/S Checkpoint Dysregulation.Toxins · 2025Article
- Semiquantitative immunohistochemical (IHC) pixelwise H-score of mitochondrial transcription factor A (TFAM) in gastric adenocarcinoma (GAC): clinicopathological significance and association with p53 and HER2.World journal of surgical oncology · 2025Article
- Cellular activity upregulation of the thermolabile p53 cancer mutant Y220C by small molecule indazole derivatives.Cell death discovery · 2025Article
- Mutant p53 as a Therapeutic Target: The Report of Its Death Was an Exaggeration.International journal of molecular sciences · 2025Review
- p53 in colorectal cancer: from a master player to a privileged therapy target.Journal of translational medicine · 2025Review
- Oncogenic and teratogenic effects ofeLife · 2025Article
- Genome-wide screening in human embryonic stem cells identifies genes and pathways involved in the p53 pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
92 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amid the complexity of genetic alterations in human cancer, TP53 mutation appears as an almost invariant component, representing by far the most frequent genetic alteration overall. Compared with previous targeted sequencing studies, recent integrated genomics studies offer a less biased view of TP53 mutation patterns, revealing that >20% of mutations occur outside the DNA-binding domain. Among the 12 mutations representing each at least 1% of all mutations, five occur at residues directly involved in specific DNA binding, four affect the tertiary fold of the DNA-binding domain, and three are nonsense mutations, two of them in the carboxyl terminus. Significant mutations also occur in introns, affecting alternative splicing events or generating rearrangements (e.g., in intron 1 in sporadic osteosarcoma). In aggressive cancers, mutation is so common that it may not have prognostic value (all these cancers have impaired p53 function caused by mutation or by other mechanisms). In several other cancers, however, mutation makes a clear difference for prognostication, as, for example, in HER2-enriched breast cancers and in lung adenocarcinoma with EGFR mutations. Thus, the clinical significance of TP53 mutation is dependent on tumor subtype and context. Understanding the clinical impact of mutation will require integrating mutation-specific information (type, frequency, and predicted impact) with data on haplotypes and on loss of heterozygosity.
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