ReviewMolecular oncology2011
p53: guardian of ploidy.
Review in Molecular oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 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
116 citing papers in PubMed, 185 citations in OpenAlex.
- Ploidy-Dependent Response to Anticancer Drugs of Human Embryonic Stem Cells.Cell proliferation · 2026Article
- Review
- Sister chromatid separation determines the proliferative properties upon whole-genome duplication via homologous chromosome arrangement.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026Review
- Human P53 Expression in Yeast: Investigating Its Apoptotic Effects.Mini reviews in medicinal chemistry · 2026Review
- Cell Fusion-Mediated Induction of Polyploidy, Aneuploidy, and Genomic Instability in Cancer Cells.Advances in experimental medicine and biology · 2026Review
- Trophoblast differentiation in the bovine placenta.The Journal of reproduction and development · 2026Review
- Genome doubling as a dynamic driver of ovarian cancer evolution: insights from single-cell sequencing.Journal of ovarian research · 2025Review
- Hepatocytes as Model for Investigating Natural Senotherapeutic Compounds and Their Effects on Cell Cycle Dynamics and Genome Stability.International journal of molecular sciences · 2025Review
- Article
- Review
- Aurora B inhibitors promote RB hypophosphorylation and senescence independent of p53-dependent CDK2/4 inhibition.Cell death & disease · 2024Article
- Polyploidy mitigates the impact of DNA damage while simultaneously bearing its burden.Cell death discovery · 2024Article
- Sumo-regulatory SENP2 controls the homeostatic squamous mitosis-differentiation checkpoint.Cell death & disease · 2024Article
- The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability.Journal of experimental & clinical cancer research : CR · 2024Article
- The antagonistic relationship between apoptosis and polyploidy in development and cancer.Seminars in cell & developmental biology · 2024Review
- DNA damage signalling histone H2AX is required for tumour growth.Cell death discovery · 2024Article
- Article
- Tetraploidization Increases the Motility and Invasiveness of Cancer Cells.International journal of molecular sciences · 2023Article
- Anti-Proliferative Effect of Radiotherapy and Implication of Immunotherapy in Anaplastic Thyroid Cancer Cells.Life (Basel, Switzerland) · 2023Article
56 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Aneuploidy, often preceded by tetraploidy, is one of the hallmarks of solid tumors. Indeed, both aneuploidy and tetraploidy are oncogenic occurrences that are sufficient to drive neoplastic transformation and cancer progression. True to form, the tumor suppressor p53 obstructs propagation of these dangerous chromosomal events by either instigating irreversible cell cycle arrest or apoptosis. The tumor suppressor Lats2, along with other tumor inhibitory proteins such as BRCA1/2 and BubR1, are central to p53-dependent elimination of tetraploid cells. Not surprisingly, these proteins are frequently inactivated or downregulated in tumors, synergizing with p53 inactivation to establish an atmosphere of "tolerance" for a non-diploid state.
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.