ReviewCancers2018
Regulators of Oncogenic Mutant TP53 Gain of Function.
Review in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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
59 citing papers in PubMed.
- KRAS and TP53 Circulating Tumor DNA are Prognostic in Localized Pancreatic Cancer.Annals of surgical oncology · 2026Article
- Case Report: A case of Lynch syndrome-related glioblastoma with coexistingFrontiers in oncology · 2026Article
- 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
- Prospective Evaluation of Circulating Tumor DNA Using Next-generation Sequencing as a Biomarker During Neoadjuvant Chemotherapy in Localized Pancreatic Cancer.Annals of surgery · 2025Article
- Transplantation outcomes of TP53-mutant AML and MDS: a single transplantation center experience of 63 patients.International journal of hematology · 2025Article
- Suppression of stress granule formation is a vulnerability imposed by mutant p53.Nature communications · 2025Article
- Polo-like kinase 2 targeting as novel strategy to sensitize mutant p53-expressing tumor cells to anticancer treatments.Journal of molecular medicine (Berlin, Germany) · 2024Article
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- Mutant TP53 promotes invasion of lung cancer cells by regulating desmoglein 3.Journal of cancer research and clinical oncology · 2024Article
- Therapeutic potential of combating cancer by restoring wild-type p53 through mRNA nanodelivery.Nanomedicine : nanotechnology, biology, and medicine · 2024Review
- Differential effect of plakoglobin in restoring the tumor suppressor activities of p53-R273H vs. p53-R175H mutants.PloS one · 2024Article
- Integrating multi-omics and machine learning survival frameworks to build a prognostic model based on immune function and cell death patterns in a lung adenocarcinoma cohort.Frontiers in immunology · 2024Article
- Association ofmedRxiv : the preprint server for health sciences · 2023Article
- Targeting Oncogenic Mutant p53 and BCL-2 for Small Cell Lung Cancer Treatment.International journal of molecular sciences · 2023Article
- Acetylation halts missense mutant p53 aggregation and rescues tumor suppression in non-small cell lung cancers.iScience · 2023Article
- Identification of an Imidazopyridine-based Compound as an Oral Selective Estrogen Receptor Degrader for Breast Cancer Therapy.Cancer research communications · 2023Article
- Impairment of rigidity sensing caused by mutant TP53 gain of function in osteosarcoma.Bone research · 2023Article
- Progressive metastatic infantile fibrosarcoma with multiple acquired mutations.Cold Spring Harbor molecular case studies · 2023Article
- Review
- Analysis of Copy Number Variation of DNA Repair/Damage Response Genes in Tumor Tissues.Methods in molecular biology (Clifton, N.J.) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The tumor suppressor p53 (TP53) is the most frequently mutated human gene. Mutations in TP53 not only disrupt its tumor suppressor function, but also endow oncogenic gain-of-function (GOF) activities in a manner independent of wild-type TP53 (wtp53). Mutant TP53 (mutp53) GOF is mainly mediated by its binding with other tumor suppressive or oncogenic proteins. Increasing evidence indicates that stabilization of mutp53 is crucial for its GOF activity. However, little is known about factors that alter mutp53 stability and its oncogenic GOF activities. In this review article, we primarily summarize key regulators of mutp53 stability/activities, including genotoxic stress, post-translational modifications, ubiquitin ligases, and molecular chaperones, as well as a single nucleotide polymorphism (SNP) and dimer-forming mutations in mutp53.
Indexed as
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.