ReviewNature reviews. Cancer2009
p53--a Jack of all trades but master of none.
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 171 papers, 3 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
171 citing papers in PubMed, 3 syntheses or guidelines pooled it, 339 citations in OpenAlex.
- The Correlation of Mouse Double Minute 4 (MDM4) Polymorphisms (rs4245739, rs1563828, rs11801299, rs10900598, and rs1380576) with Cancer Susceptibility: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2022Pooled it
- The associations between MDM4 gene polymorphisms and cancer risk.Oncotarget · 2016Pooled it
- Prognostic significance of p53 expression in malignant bone tumors: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Pooled it
- The impact of functional MDM2-polymorphisms on neutrophil counts in breast cancer patients during neoadjuvant chemotherapy.BMC cancer · 2025Trial
- Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- Epstein-Barr Virus-Mediated Apoptosis Evasion in Epithelial Malignancies: Molecular Mechanisms and Therapeutic Implications.Biology · 2026Review
- Making Sense of Missense: Assessing and Incorporating the Functional Impact of Constitutional Genetic Testing.Children (Basel, Switzerland) · 2025Article
- Advances in the anti-tumor mechanisms of saikosaponin D.Pharmacological reports : PR · 2024Review
- A stumbling block in pancreatic cancer treatment: drug resistance signaling networks.Frontiers in cell and developmental biology · 2024Review
- Next-Cell Hypothesis: Mechanism of Obesity-Associated Carcinogenesis.Advances in experimental medicine and biology · 2024Review
- Evolutionary determinants of curability in cancer.Nature ecology & evolution · 2023Review
- Convergent TP53 loss and evolvability in cancer.BMC ecology and evolution · 2023Review
- Kinesin superfamily member 15 knockdown inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- Pharmacological inhibition of MDM4 alleviates pulmonary fibrosis.Theranostics · 2023Article
- YAP1 and P53 Expression in Papillary Thyroid Carcinoma.Iranian journal of pathology · 2023Article
- Myelodysplastic Syndromes with Isolated del(5q): Value of Molecular Alterations for Diagnostic and Prognostic Assessment.Cancers · 2022Review
- Iron metabolism, ferroptosis, and lncRNA in cancer: knowns and unknowns.Journal of Zhejiang University. Science. B · 2022Review
- Synthesis and Biological Evaluation of Indole-2-Carboxamides with Potent Apoptotic Antiproliferative Activity as EGFR/CDK2 Dual Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Call the Eckols: Present and Future Potential Cancer Therapies.Marine drugs · 2022Review
- Molecular Insights into Oral Malignancy.Indian journal of surgical oncology · 2022Review
111 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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancers are rare because their evolution is actively restrained by a range of tumour suppressors. Of these p53 seems unusually crucial as either it or its attendant upstream or downstream pathways are inactivated in virtually all cancers. p53 is an evolutionarily ancient coordinator of metazoan stress responses. Its role in tumour suppression is likely to be a relatively recent adaptation, which is only necessary when large, long-lived organisms acquired the sufficient size and somatic regenerative capacity to necessitate specific mechanisms to reign in rogue proliferating cells. However, such evolutionary reappropriation of this venerable transcription factor entails compromises that restrict its efficacy as a tumour suppressor.
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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.