ReviewTrends in genetics : TIG2018
Transposons, p53 and Genome Security.
Review in Trends in genetics : TIG, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 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
32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 citations in OpenAlex.
- Role of the STING pathway in myeloid neoplasms: a prospero-registered systematic review of principal hurdles of STING on the road to the clinical practice.Medical oncology (Northwood, London, England) · 2024Pooled it
- Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023Pooled it
- PARP1 inhibition in naïve mouse embryonic stem cells induces viral mimicry.Nucleic acids research · 2026Article
- MORC2 promotes acute myeloid leukemia by silencing LINE-1 retrotransposon.Functional & integrative genomics · 2026Article
- The Chromaverse Is Colored by Triplexes Formed Through the Interactions of Noncoding RNAs with HNPRNPU, TP53, AGO, REL Proteins, Intrinsically-Disordered Regions, and Flipons.International journal of molecular sciences · 2026Article
- Retroelements in thyroid cancer: epigenetic plasticity, dedifferentiation, and therapeutic opportunities.Reviews in endocrine & metabolic disorders · 2026Review
- Estrogen-Driven Breast Carcinogenesis in a Rat Model is Linked to Retroelement Activation and Inflammation and is Susceptible to Lamivudine Treatment.Breast cancer (Dove Medical Press) · 2026Article
- Cell state dynamics during early stages of serous endometrial carcinoma.The Journal of pathology · 2025Article
- Transposable elements in health and disease: Molecular basis and clinical implications.Chinese medical journal · 2025Review
- Retrotransposon methylation profiles and survival in Black women with high-grade serous ovarian carcinoma.Clinical epigenetics · 2025Article
- Cancer cell type-specific derepression of transposable elements by inhibition of chromatin modifier enzymes.Communications biology · 2025Article
- TP53-Mutated Acute Myeloid Leukemia: Unanswered Questions.Hematological oncology · 2025Review
- p53motifDB: integration of genomic information and tumour suppressor p53 binding motifs.Database : the journal of biological databases and curation · 2025Article
- IRE1α silences dsRNA to prevent taxane-induced pyroptosis in triple-negative breast cancer.Cell · 2024Article
- Repetitive element transcript accumulation is associated with inflammaging in humans.GeroScience · 2024Article
- Cell-free DNA from germline TP53 mutation carriers reflect cancer-like fragmentation patterns.Nature communications · 2024Article
- Bioactive Components of Areca Nut: An Overview of Their Positive Impacts Targeting Different Organs.Nutrients · 2024Review
- Transposable elements as tissue-specific enhancers in cancers of endodermal lineage.Nature communications · 2023Article
- Ribosomal protein mutations and cell competition: autonomous and nonautonomous effects on a stress response.Genetics · 2023Article
- Pan-cancer analysis identifies tumor-specific antigens derived from transposable elements.Nature genetics · 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
3 authors at 1 institution in 1 country.
Funding
Abstract
p53, the most commonly mutated tumor suppressor, is a transcription factor known to regulate proliferation, senescence, and apoptosis. Compelling studies have found that p53 may prevent oncogenesis through effectors that are unrelated to these canonical processes and recent findings have uncovered ancient roles for p53 in the containment of mobile elements. Together, these developments raise the possibility that some p53-driven cancers could result from unrestrained transposons. Here, we explore evidence linking conserved features of p53 biology to the control of transposons. We also show how p53-deficient cells can be exploited to probe the behavior of transposons and illustrate how unrestrained transposons incited by p53 loss might contribute to human malignancies.
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.