ReviewFrontiers in oncology2016
Mutant p53 and ETS2, a Tale of Reciprocity.
Review in Frontiers in oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 29 citations in OpenAlex.
- Single-cell atlas of hepatic cellular plasticity and immune niche reprogramming in liver cirrhosis.Journal of translational medicine · 2026Article
- Uncovering the role of ETS2 in prostate cancer pathogenesis: relationship with p53 and ERG.Molecular biology reports · 2026Article
- Sepsis-induced acute lung injury: AUF1 regulates pyroptosis via ETS2/ZDHHC21-mediated STING palmitoylation : A therapeutic target for lung injury.Cellular and molecular life sciences : CMLS · 2025Article
- ETS2 aggravate allergic airway inflammation by regulating ANT2-mediated cytosolic mitochondrial DsRNA levels.Respiratory research · 2025Article
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- Unveiling the link between arsenic toxicity and diabetes: an in silico exploration into the role of transcription factors.Toxicological research · 2024Article
- Article
- Domain-specific p53 mutants activate EGFR by distinct mechanisms exposing tissue-independent therapeutic vulnerabilities.Nature communications · 2023Article
- Interpretable deep learning for chromatin-informed inference of transcriptional programs driven by somatic alterations across cancers.Nucleic acids research · 2022Article
- Immune cells transcriptome-based drug repositioning for multiple sclerosis.Frontiers in immunology · 2022Article
- lncRNA DLEU2 promotes gastric cancer progression through ETS2 via targeting miR-30a-5p.Cancer cell international · 2021Article
- Review
- Dynamics of m6A RNA Methylome on the Hallmarks of Hepatocellular Carcinoma.Frontiers in cell and developmental biology · 2021Review
- p53 Loss Mediates Hypersensitivity to ETS Transcription Factor Inhibition Based on PARylation-Mediated Cell Death Induction.Cancers · 2020Article
- Development of a CDK10/CycMFrontiers in chemistry · 2020Article
- The Diverse Functions of Mutant 53, Its Family Members and Isoforms in Cancer.International journal of molecular sciences · 2019Review
- ETS2 is a prostate basal cell marker and is highly expressed in prostate cancers aberrantly expressing p63.The Prostate · 2018Article
- Tracing the path of cancer initiation: the AA protein-based model for cancer genesis.BMC cancer · 2018Article
- Aberrant expression of ETS1 and ETS2 proteins in cancer.Cancer reports and reviews · 2018Article
- Control of Nucleotide Metabolism Enables Mutant p53's Oncogenic Gain-of-Function Activity.International journal of molecular sciences · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
TP53 is one of the most frequently inactivated tumor suppressor genes in human cancer. However, unlike other tumor suppressor genes whose expression is lost, TP53 is usually inactivated as a result of a single nucleotide change within the coding region. Typically, these single nucleotide mutations result in a codon change that creates an amino acid substitution. Thus, unlike other tumor suppressor genes whose expression is lost due to genetic or epigenetic changes, the p53 gene primarily suffers missense mutations, and therefore, the cells retain and express a mutant form of the p53 protein (mtp53). It is now well established that mtp53 contributes to tumor development through its gain-of-function (GOF) activities. These GOF activities can arise from novel protein-protein interactions that can either disable other tumor suppressors (e.g., p63 and p73) or enable oncogenes such as ETS2, an ETS family member. In this review, I will focus on the identification of the mtp53/ETS2 complex and outline the diverse activities that this transcriptional regulatory complex controls to promote cancer.
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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.