ReviewJournal of molecular biology2017
Mutant p53 in Cancer: Accumulation, Gain-of-Function, and Therapy.
Review in Journal of molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 papers, 4 of them syntheses that pooled it.
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
172 citing papers in PubMed, 4 syntheses or guidelines pooled it, 308 citations in OpenAlex.
- Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023Pooled it
- Germline and Somatic Genetic Variants in the p53 Pathway Interact to Affect Cancer Risk, Progression, and Drug Response.Cancer research · 2021Pooled it
- High expression of SPP1 in patients with chronic obstructive pulmonary disease (COPD) is correlated with increased risk of lung cancer.FEBS open bio · 2021Pooled it
- Immune Infiltration Landscape in Lung Squamous Cell Carcinoma Implications.BioMed research international · 2020Pooled it
- Correlative assessment of p53 immunostaining patterns and TP53 mutation status by next-generation sequencing in lung adenocarcinoma (LUAD).Histopathology · 2026Article
- Review
- Investigating the anticancer activity of eravacycline in pancreatic cancer via target-based deep learning and experimental validation.Briefings in bioinformatics · 2026Article
- Genomic Enrichment and Functional Impact of TP53 and CYLD Alterations in Recurrent and Metastatic HPV-Associated Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Targeting mutant p53 in cancer: from mechanistic insights to therapeutic strategies.Cellular & molecular biology letters · 2026Review
- The MDM2-p53 Axis in Osteosarcoma: Current Understanding of Regulatory Mechanisms and Targeted Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Pro-ATO/Allicin Liposomes for Dual-Pathway Targeting of p53-Mutant Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Deciphering molecular pathways in urological cancers: A gateway to precision therapeutics.Journal of advanced research · 2026Review
- Probiotic and microbial modulation of polyamine production: an emerging avenue for neuroprotection in neurodegenerative disorders.Amino acids · 2026Review
- Benzodioxin-Annulated Naphthalimides as Potent DNA Replication Stress Inducers with Dual p53-Dependent and Independent Antitumor Activity.Pharmaceutics · 2026Article
- Low-VAF TP53-Mutated AML Displays Distinct Biological Features in a Single-Center Cohort.Biomedicines · 2026Article
- Biology of p53 protein isoforms and their significance in hematological malignancies.Frontiers in oncology · 2026Review
- Periosteal Osteosarcoma: Emerging Clinical Concepts, Evolving Treatment Options: A Narrative Review.Current pain and headache reports · 2025Review
- Non-invasive prediction of Ki-67 and p53 biomarkers in spinal ependymoma via deep learning: using multimodal magnetic resonance imaging and clinical data.Biomarker research · 2025Article
- Propofol inhibits glioma growth by blocking the formation of the NF-κB/LGI4 feedback loop to activate TP53 self-transcription.Translational oncology · 2025Article
- Recent advances in metal ions overloading for tumors: Mechanisms, nanomaterials, and therapies.Materials today. Bio · 2025Review
112 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
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Tumor suppressor p53 plays a central role in tumor suppression. p53 is the most frequently mutated gene in human cancer, and over half of human cancers contain p53 mutations. Majority of p53 mutations in cancer are missense mutations, leading to the expression of full-length mutant p53 (mutp53) protein. While the critical role of wild-type p53 in tumor suppression has been firmly established, mounting evidence has demonstrated that many tumor-associated mutp53 proteins not only lose the tumor-suppressive function of wild-type p53 but also gain new activities to promote tumorigenesis independently of wild-type p53, termed gain-of-function. Mutant p53 protein often accumulates to very high levels in tumors, contributing to malignant progression. Recently, mutp53 has become an attractive target for cancer therapy. Further understanding of the mechanisms underlying mutp53 protein accumulation and gain-of-function will accelerate the development of targeted therapies for human cancer harboring mutp53. In this review, we summarize the recent advances in the studies on mutp53 protein accumulation and gain-of-function and targeted therapies for mutp53 in human cancer.
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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.