ReviewOncogenesis2016
Gain of function of mutant p53: R282W on the peak?
Review in Oncogenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- Covalent drug rescue of multiple p53 mutants by stabilizing vinyl sulfone fragments hints to a specific refolding mechanism for R282W.Protein science : a publication of the Protein Society · 2026Article
- Targeting mutant p53 in cancer: from mechanistic insights to therapeutic strategies.Cellular & molecular biology letters · 2026Review
- Transfer Learning for Survival-based Clustering of Predictors with an Application tobioRxiv : the preprint server for biology · 2025Article
- Mutational Disruption of TP53: A Structural Approach to Understanding Chemoresistance.International journal of molecular sciences · 2025Article
- Frustration in physiology and molecular medicine.Molecular aspects of medicine · 2025Review
- Chromatin Immunoprecipitation Reveals p53 Binding to G-Quadruplex DNA Sequences in Myeloid Leukemia Cell Lines.ACS bio & med chem Au · 2025Article
- Lipid nanoparticles deliver DNA-encoded biologics and induce potent protective immunity.Molecular cancer · 2025Article
- Loss of phosphatase and tensin homolog (Cancer pathogenesis and therapy · 2025Article
- Review
- Somatic mutations in facial skin from countries of contrasting skin cancer risk.Nature genetics · 2023Article
- Homogenous TP53mut-associated tumor biology across mutation and cancer types revealed by transcriptome analysis.Cell death discovery · 2023Article
- Long noncoding RNA LINC01088 inhibits esophageal squamous cell carcinoma progression by targeting the NPM1-HDM2-p53 axis.Acta biochimica et biophysica Sinica · 2023Article
- Somatic mutation detection andFrontiers in oncology · 2023Article
- Conformational Heterogeneity and Frustration of the Tumor Suppressor p53 as Tuned by Punctual Mutations.International journal of molecular sciences · 2022Article
- Clinical applications of liquid biopsy in HPV-negative and HPV-positive head and neck squamous cell carcinoma: advances and challenges.Exploration of targeted anti-tumor therapy · 2022Review
- RNA-SSNV: A Reliable Somatic Single Nucleotide Variant Identification Framework for Bulk RNA-Seq Data.Frontiers in genetics · 2022Article
- Regulation of Neuroendocrine-like Differentiation in Prostate Cancer by Non-Coding RNAs.Non-coding RNA · 2021Review
- Structural and Drug Targeting Insights on Mutant p53.Cancers · 2021Review
- Ring finger 20/ring finger 40/WW domain-containing adaptor with coiled-coil complex interacts with p53 to regulate gene transcription in DNA damage response.Oncology letters · 2021Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutant p53 proteins commonly lose their tumor suppression function and gain novel oncogenic functions (gain of function (GOF)). Different p53 mutations are often considered in one class in biological and clinical studies. However, recent studies have revealed that p53 mutations are biologically and clinically distinct. The R282W mutant associates with earlier onset of familial cancers and poorer outcome of cancer patients, suggesting a more prominent GOF effect of this specific mutant. Here we discuss our current understanding on the multifaceted effects of R282W mutation, including its structural features, signaling pathways and clinical implications. The destabilizing nature, aggregation proneness, altered transcriptome and interactome may collaboratively contribute to the unique phenotype of R282W mutation. The quest for mechanistic insights into the unique GOF effects of R282W mutation would further our understanding of the biology of mutant proteins in cancers, and enforce the development of more effective targeted therapies.
Identifiers
What OpenQuestion holds
Registered trials
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.