ReviewOncogene2007
p53 alterations in human cancer: more questions than answers.
Review in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 4 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
100 citing papers in PubMed, 4 syntheses or guidelines pooled it, 231 citations in OpenAlex.
- Value of p53 sequencing in the prognostication of head and neck cancer: a systematic review and meta-analysis.Scientific reports · 2022Pooled it
- Clinicopathologic characteristics of brain tumors are associated with the presence and patterns of TP53 mutations: evidence from the IARC TP53 Database.Neuromolecular medicine · 2014Pooled it
- p53 status and its prognostic role in extrahepatic bile duct cancer: a meta-analysis of published studies.Digestive diseases and sciences · 2011Pooled it
- A systematic review of p53 as a prognostic factor of survival in squamous cell carcinoma of the four main anatomical subsites of the head and neck.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2010Pooled it
- Associations between p53 overexpression and multiple measures of clinical outcome in high-risk, early stage or suboptimally-resected, advanced stage epithelial ovarian cancers A Gynecologic Oncology Group study.Gynecologic oncology · 2008Trial
- An integrative approach to studying sphingolipid metabolism reveals p53 as a master regulator of the pathway.Journal of lipid research · 2026Article
- Clinical Relevance ofCancers · 2024Article
- p53 protein expression patterns associated with TP53 mutations in breast carcinoma.Breast cancer research and treatment · 2024Article
- Canonical and non-canonical functions of p53 isoforms: potentiating the complexity of tumor development and therapy resistance.Cell death & disease · 2024Review
- Updates on Larynx Cancer: Risk Factors and Oncogenesis.International journal of molecular sciences · 2023Review
- miR-221/222 induce instability of p53 By downregulating deubiquitinase YOD1 in acute myeloid leukemia.Cell death discovery · 2023Article
- A Brief Review on Chemoresistance; Targeting Cancer Stem Cells as an Alternative Approach.International journal of molecular sciences · 2023Review
- Analysis of Intrinsic Breast Cancer Subtypes: The Clinical Utility of Epigenetic Biomarkers andInternational journal of molecular sciences · 2022Article
- Alterations in p53 Influence hTERT, VEGF and MMPs Expression in Oral Cancer Patients.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Distinct p53 isoforms code for opposing transcriptional outcomes.Developmental cell · 2022Article
- Generation of a uniform thymic malignant lymphoma model with C57BL/6JJournal of toxicologic pathology · 2022Article
- p53-Mediated Indirect Regulation on Cellular Metabolism: From the Mechanism of Pathogenesis to the Development of Cancer Therapeutics.Frontiers in oncology · 2022Review
- Sphingolipid metabolism in the development and progression of cancer: one cancer's help is another's hindrance.Molecular oncology · 2021Review
- KLF5 regulates epithelial-mesenchymal transition of liver cancer cells in the context of p53 loss through miR-192 targeting of ZEB2.Cell adhesion & migration · 2020Article
- Characterization of Exosomes in Plasma of Patients with Breast, Ovarian, Prostate, Hepatic, Gastric, Colon, and Pancreatic Cancers.Journal of cancer therapy · 2019Article
40 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
1 author at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The strongest and undisputed fact about p53 is the high frequency of p53 alterations in human cancer and that mutant p53 proteins constitute a complex family of several hundred proteins with heterogeneous properties. Beyond these observations, the p53 pathway and its regulation in a normal cell is like a desert trail, always moving with the wind of novel findings. The field is full of black boxes that are often ignored for sake of simplicity or because they do not fit with the current dominant view. Mutant p53 protein accumulation in tumours is the best example of a preconceived idea, as there is no experimental evidence to explain this observation. In this review, we will discuss several questions concerning the activity or selection of p53 mutations. The central domain of the p53 protein targeted by 80% of p53 mutations is associated with the DNA-binding activity of the p53 protein, but it is also the binding site for several proteins that play a key role in p53 regulation such as ASPP proteins or BclxL. The role of impaired DNA binding and/or protein interactions in tumour development has not been fully elucidated. Similarly, novel animal models carrying either missense p53 mutations or inducible p53 have provided abundant observations, some of which could challenge our view on p53 function as a tumour suppressor gene. Finally, the possible clinical applications of p53 will be discussed.
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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.