ReviewCell death and differentiation2022
Of the many cellular responses activated by TP53, which ones are critical for tumour suppression?
Review in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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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.
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Who cites it
66 citing papers in PubMed, 99 citations in OpenAlex.
- Switches in alternatively spliced isoforms impact protein and drug interactions in melanoma, ovarian cancer, and acute myeloid leukemia.British journal of cancer · 2026Article
- Integrated Transcriptomic and Metabolomic Analysis Reveals the Regulatory Mechanisms ofBiology · 2026Article
- Integrating Network Toxicology with Molecular Dynamics Simulations to Reveal Key Targets and Binding Mechanisms of Bisphenol A in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2026Article
- Aging and cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- Nuclear adenosine metabolism defines a metabolic vulnerability unmasked by TP53 loss.bioRxiv : the preprint server for biology · 2026Article
- TP53 mutation is associated with shorter treatment duration with CDK4/6 inhibitors, but not with immune checkpoint inhibitors, in ER-positive/HER2-negative breast cancer: real-world perspective.Breast cancer research : BCR · 2026Article
- Integrative In Silico Identification of TP53-Associated Drug Repurposing Candidates in Lung Adenocarcinoma.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Combined Inhibition of ATR and Ribonucleotide Reductase Induces Synergistic Antineoplastic Activity in Osteosarcoma Cells.Cancer reports (Hoboken, N.J.) · 2026Article
- Targeting STAT5A via CRISPR/Cas9 restores TKI sensitivity in resistant chronic myeloid leukemia cells.Medical oncology (Northwood, London, England) · 2026Article
- PRDM16 protects retinal ganglion cells from ischemia-reperfusion Injury by regulating the RPL5/p53 axis.Cellular and molecular life sciences : CMLS · 2026Article
- Chromatin-associated circRNA ciCRLF3(2) regulates cell differentiation blockage via activating non-homologous end joining-based DNA repair.Cell death and differentiation · 2026Article
- The value of DNA repair gene and TP53 co-mutation in predicting the response of non-small cell lung cancer to immunotherapy.Discover oncology · 2026Article
- Identification of DNA Replication Stress-Related Genes as Prognostic Biomarkers for Bladder Cancer.Combinatorial chemistry & high throughput screening · 2026Article
- Pandora's Box of AML: HowBiomedicines · 2025Review
- Deacetylation of ACLY Mediates RNA MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Multi-omic characterization of consensus molecular subtype 1 (CMS1) colorectal cancer with dampened immune response improves precision medicine.Molecular oncology · 2025Article
- Leveraging the htsFLT01/MiRGD Complex to Enhance Apoptosis and Suppress Angiogenesis in MCF7 Breast Cancer Cells.Iranian journal of medical sciences · 2025Article
- Article
- Death-ision: the link between cellular resilience and cancer resistance to treatments.Molecular cancer · 2025Review
- Exploring the Genetic Orchestra of Cancer: The Interplay Between Oncogenes and Tumor-Suppressor Genes.Cancers · 2025Review
6 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumour suppressor TP53 is a master regulator of several cellular processes that collectively suppress tumorigenesis. The TP53 gene is mutated in ~50% of human cancers and these defects usually confer poor responses to therapy. The TP53 protein functions as a homo-tetrameric transcription factor, directly regulating the expression of ~500 target genes, some of them involved in cell death, cell cycling, cell senescence, DNA repair and metabolism. Originally, it was thought that the induction of apoptotic cell death was the principal mechanism by which TP53 prevents the development of tumours. However, gene targeted mice lacking the critical effectors of TP53-induced apoptosis (PUMA and NOXA) do not spontaneously develop tumours. Indeed, even mice lacking the critical mediators for TP53-induced apoptosis, G1/S cell cycle arrest and cell senescence, namely PUMA, NOXA and p21, do not spontaneously develop tumours. This suggests that TP53 must activate additional cellular responses to mediate tumour suppression. In this review, we will discuss the processes by which TP53 regulates cell death, cell cycling/cell senescence, DNA damage repair and metabolic adaptation, and place this in context of current understanding of TP53-mediated tumour suppression.
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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.