ReviewInternational journal of molecular sciences2019
Gain-of-Function Mutant p53: All the Roads Lead to Tumorigenesis.
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 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
98 citing papers in PubMed.
- The Dual Role of Ferroptosis in Cancer: Molecular Mechanisms, Microenvironment Crosstalk, and Precision Therapeutics.Cancers · 2026Review
- Isolation and identification of a highly oncogenic subgroup J avian leukosis virus strain from Chinese black chickens.Poultry science · 2026Article
- Mutant p53 Regulates Pyruvate Dehydrogenase Kinase 1 (PDK1) to Promote Proliferation and Migration in Breast Cancer.Cancer science · 2026Article
- The p53 R181C mutation accumulates through impaired deacetylation by Sirt1 and facilitates tumor development.Communications biology · 2026Article
- Tumor Suppressor p53 and MicroRNAs Interaction in Breast Cancer.Oncology research · 2026Review
- Small molecules that targeting p53 Y220C protein: mechanisms, structures, and clinical advances in anti-tumor therapy.Molecular diversity · 2025Review
- A cancer persistent DNA repair circuit driven by MDM2, MDM4 (MDMX), and mutant p53 for recruitment of MDC1 and 53BP1 on chromatin.Nucleic acids research · 2025Article
- Integrated analysis of oral rinse-derived and plasma circulating tumour DNA for mutation profiling and outcome prediction with oral squamous cell carcinoma.NPJ precision oncology · 2025Article
- Review
- Review
- The Role of p53 Mutations in Early and Late Response to Mitotic Aberrations.Biomolecules · 2025Review
- dbGVOSCC: a comprehensive database of genetic variation for systems genetics research on oral squamous cell carcinoma.Frontiers in oncology · 2025Article
- Identification of a novel prognostic marker ADGRG6 in pancreatic adenocarcinoma: multi-omics analysis and experimental validation.Frontiers in immunology · 2025Article
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- Current insights and future directions of Li-Fraumeni syndrome.Discover oncology · 2024Review
- MIR193BHG inhibits the proliferation, migration and invasion of trophoblasts by upregulating p53.Experimental and therapeutic medicine · 2024Article
- The influence of a modified p53 C-terminal peptide by using a tumor-targeting sequence on cellular apoptosis and tumor treatment.Apoptosis : an international journal on programmed cell death · 2024Article
- Ferulic acid interventions ameliorate NDEA-CClToxicology reports · 2024Article
- Review
- Multidimensional pan-cancer analysis of HSPA5 and its validation in the prognostic value of bladder cancer.Heliyon · 2024Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The p53 protein is mutated in about 50% of human cancers. Aside from losing the tumor-suppressive functions of the wild-type form, mutant p53 proteins often acquire inherent, novel oncogenic functions, a phenomenon termed mutant p53 gain-of-function (GOF). A growing body of evidence suggests that these pro-oncogenic functions of mutant p53 proteins are mediated by affecting the transcription of various genes, as well as by protein-protein interactions with transcription factors and other effectors. In the current review, we discuss the various GOF effects of mutant p53, and how it may serve as a central node in a network of genes and proteins, which, altogether, promote the tumorigenic process. Finally, we discuss mechanisms by which "Mother Nature" tries to abrogate the pro-oncogenic functions of mutant p53. Thus, we suggest that targeting mutant p53, via its reactivation to the wild-type form, may serve as a promising therapeutic strategy for many cancers that harbor mutant p53. Not only will this strategy abrogate mutant p53 GOF, but it will also restore WT p53 tumor-suppressive functions.
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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.