ReviewCancers2021
Dying to Survive-The p53 Paradox.
Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 35 citations in OpenAlex.
- Chronic low-dose iron exposure induces GPX4-mediated resistance to ferroptosis in a human chondrocyte cell line.Cell and tissue research · 2026Article
- The Enigmatic Tumor Suppressor p53 Biomolecule: Its Role and Prognostic and Predictive Values in Cancer Therapy and Precision Medicine.Biomolecules · 2026Review
- TAK1 inhibition restores p53 expression and suppresses inflammation and hyperplasia in JIA synovial fibroblasts.Rheumatology (Oxford, England) · 2026Article
- The Oncogenic Role of Long Non-Coding RNABiology · 2026Review
- HIF1α mediates resistance to radiation and to KRAS inhibitors in pancreatic adenocarcinoma.PloS one · 2026Article
- What Is Apoptosis and Why Is It Inhibited by the Most Important Tumor Suppressor (p53)?International journal of molecular sciences · 2025Review
- Harnessing p53 for targeted cancer therapy: new advances and future directions.Transcription · 2025Review
- Biomarker Profiles and Clinicopathological Features in Head and Neck Squamous Cell Carcinoma Patients.Medicina (Kaunas, Lithuania) · 2024Article
- Targeting tumor suppressor p53 for organ fibrosis therapy.Cell death & disease · 2024Review
- Neuroprotective Effect of Sterculia setigera Leaves Hydroethanolic Extract.Journal of molecular neuroscience : MN · 2024Article
- Transcriptional pausing induced by ionizing radiation enables the acquisition of radioresistance in nasopharyngeal carcinoma.Journal of molecular cell biology · 2024Article
- Differential effect of plakoglobin in restoring the tumor suppressor activities of p53-R273H vs. p53-R175H mutants.PloS one · 2024Article
- Article
- Evaluation of the p53 pathway in polycystic ovarian syndrome pathogenesis and apoptosis enhancement in human granulosa cells through transcriptome data analysis.Scientific reports · 2023Article
- Diepoxybutane induces the p53-dependent transactivation of the CCL4 gene that mediates apoptosis in exposed human lymphoblasts.Journal of biochemical and molecular toxicology · 2023Article
- Single-cell sequencing of tumor-associated macrophages in aFrontiers in immunology · 2023Article
- Low Sulfur Amino Acid, High Polyunsaturated Fatty Acid Diet Inhibits Breast Cancer Growth.International journal of molecular sciences · 2022Article
- DNA damage response revisited: the p53 family and its regulators provide endless cancer therapy opportunities.Experimental & molecular medicine · 2022Review
- Banp regulates DNA damage response and chromosome segregation during the cell cycle in zebrafish retina.eLife · 2022Article
- Interdiction in the Early Folding of the p53 DNA-Binding Domain Leads to Its Amyloid-Like Misfolding.Molecules (Basel, Switzerland) · 2022Article
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
The p53 tumour suppressor is best known for its canonical role as "guardian of the genome", activating cell cycle arrest and DNA repair in response to DNA damage which, if irreparable or sustained, triggers activation of cell death. However, despite an enormous amount of work identifying the breadth of the gene regulatory networks activated directly and indirectly in response to p53 activation, how p53 activation results in different cell fates in response to different stress signals in homeostasis and in response to p53 activating anti-cancer treatments remains relatively poorly understood. This is likely due to the complex interaction between cell death mechanisms in which p53 has been activated, their neighbouring stressed or unstressed cells and the local stromal and immune microenvironment in which they reside. In this review, we evaluate our understanding of the burgeoning number of cell death pathways affected by p53 activation and how these may paradoxically suppress cell death to ensure tissue integrity and organismal survival. We also discuss how these functions may be advantageous to tumours that maintain wild-type p53, the understanding of which may provide novel opportunity to enhance treatment efficacy.
Indexed as
Identifiers
What Socratic 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 Socratic graph.