ReviewNature reviews. Cancer2009
p53 and E2f: partners in life and death.
Review in Nature reviews. Cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 279 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
279 citing papers in PubMed, 2 syntheses or guidelines pooled it, 490 citations in OpenAlex.
- Association of theDisease markers · 2016Pooled it
- Association between TP53 Arg72Pro polymorphism and thyroid carcinoma risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- E2F1 Drives Endothelial Arterial Programming in Pulmonary Arterial Hypertension.bioRxiv : the preprint server for biology · 2026Article
- Pro-apoptotic and cell cycle-modulating effects of lobaric and rhizocarpic acids in human leukemic cell lines.Molecular biology reports · 2026Article
- Exploring the Research Progress of Vascular Dementia and Key Regulatory Molecules: E2F1.International journal of molecular sciences · 2026Review
- Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression.Cancer immunology research · 2025Article
- MUC1-C auto-regulatory complex with EBNA1 is responsible for latent Epstein-Barr virus-associated gastric cancer progression.Oncogene · 2025Article
- A Nanostring gene expression approach identifies aggressive clinical behavior related genes in dedifferentiated liposarcoma.Scientific reports · 2025Article
- CENPF (+) cancer cells promote malignant progression of early-stage TP53 mutant lung adenocarcinoma.Oncogenesis · 2025Article
- KRASCell reports. Medicine · 2025Article
- Acetylation of E2F1 at K125 facilitates cell apoptosis under serum stress.Translational oncology · 2025Article
- The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025Review
- NEK2 inhibition alleviates lipopolysaccharide-induced endothelial injury.ASPET discovery · 2025Article
- Anticancer effects and mechanisms ofComputational and structural biotechnology journal · 2025Article
- Uncovering the anticancer effects of Bhallataka Taila in lung cancer: A metabolomic and network pharmacology approach.BioImpacts : BI · 2025Article
- DEAD/H Box 5 (DDX5) Augments E2F1-Induced Cell Death Independent of the Tumor Suppressor p53.International journal of molecular sciences · 2024Article
- TRIM-endous functional network of tripartite motif 29 (TRIM29) in cancer progression and beyond.Cancer metastasis reviews · 2024Review
- Article
- The N-Terminal Region of the Transcription Factor E2F1 Contains a Novel Transactivation Domain and Recruits General Transcription Factor GTF2H2.Biomolecules · 2024Article
- Rapamycin Attenuates HTissue engineering and regenerative medicine · 2024Article
219 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
No grant is acknowledged in the PubMed record.
Abstract
During tumour development cells sustain mutations that disrupt normal mechanisms controlling proliferation. Remarkably, the Rb-E2f and MDM2-p53 pathways are both defective in most, if not all, human tumours, which underscores the crucial role of these pathways in regulating cell cycle progression and viability. A simple interpretation of the observation that both pathways are deregulated is that they function independently in the control of cell fate. However, a large body of evidence indicates that, in addition to their independent effects on cell fate, there is extensive crosstalk between these two pathways, and specifically between the transcription factors E2F1 and p53, which influences vital cellular decisions. This Review discusses the molecular mechanisms that underlie the intricate interactions between E2f and p53.
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.