ReviewInternational journal of molecular sciences2021
At a Crossroads to Cancer: How p53-Induced Cell Fate Decisions Secure Genome Integrity.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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
39 citing papers in PubMed, 61 citations in OpenAlex.
- Mitotic errors as triggers of cell death and inflammation.Nature cell biology · 2026Review
- PUMA-induced apoptosis drives bone marrow failure and genomic instability in telomerase-deficient mice.Cell death and differentiation · 2026Article
- Multi-Level Profiling of MAPK-Associated Genes and MicroRNAs Uncovers Regulatory Networks in Breast Cancer Subtypes.International journal of molecular sciences · 2025Article
- Dominant-Negative Effects of p53 R337 Variants in Li-Fraumeni Syndrome: Impact on Tetramer Formation and Transcriptional Activity.Chembiochem : a European journal of chemical biology · 2025Article
- Defining the transcriptional routes controlling lncRNA NEAT1 expression: implications in cellular stress response, inflammation, and differentiation.Discover oncology · 2025Review
- Inorganic Arsenic Induces Elevated p53 Levels with Altered Functionality Impacting the Expression of Toll-like Receptor 3 and Other Target Genes in Immortalized Prostate Epithelial Cells.International journal of molecular sciences · 2025Article
- Cyclin C promotes development and progression of B-cell acute lymphoblastic leukemia by counteracting p53-mediated stress responses.Haematologica · 2025Article
- The anticancer effects of Aronia berry extract are mediated by Chk1 and p53 in colorectal cancer.Phytomedicine : international journal of phytotherapy and phytopharmacology · 2024Article
- PKMYT1 Is a Marker of Treatment Response and a Therapeutic Target for CDK4/6 Inhibitor-Resistance in ER+ Breast Cancer.Molecular cancer therapeutics · 2024Article
- Dominant suppressor genes of p53-induced apoptosis in Drosophila melanogaster.G3 (Bethesda, Md.) · 2024Article
- Functional evaluation of germline TP53 variants identified in Brazilian families at-risk for Li-Fraumeni syndrome.Scientific reports · 2024Article
- Effect and mechanism of resveratrol on ferroptosis mediated by p53/SLC7A11 in oral squamous cell carcinoma.BMC oral health · 2024Article
- Mcph1, mutated in primary microcephaly, is also crucial for erythropoiesis.EMBO reports · 2024Article
- From Cell Populations to Molecular Complexes: Multiplexed Multimodal Microscopy to Explore p53-53BP1 Molecular Interaction.International journal of molecular sciences · 2024Article
- Molecular mechanism of human ISG20L2 for the ITS1 cleavage in the processing of 18S precursor ribosomal RNA.Nucleic acids research · 2024Article
- Quercetin, a Flavonoid with Great Pharmacological Capacity.Molecules (Basel, Switzerland) · 2024Review
- Exploring the Role of Globular Domain Locations on an Intrinsically Disordered Region of p53: A Molecular Dynamics Investigation.Journal of chemical theory and computation · 2024Article
- Transcriptional pausing induced by ionizing radiation enables the acquisition of radioresistance in nasopharyngeal carcinoma.Journal of molecular cell biology · 2024Article
- Titanium dioxide nanostructure-loaded Adriamycin surmounts resistance in breast cancer therapy: ABCA/P53/C-myc crosstalk.Future science OA · 2024Article
- SIRT7: the seventh key to unlocking the mystery of aging.Physiological reviews · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
P53 is known as the most critical tumor suppressor and is often referred to as the guardian of our genome. More than 40 years after its discovery, we are still struggling to understand all molecular details on how this transcription factor prevents oncogenesis or how to leverage current knowledge about its function to improve cancer treatment. Multiple cues, including DNA-damage or mitotic errors, can lead to the stabilization and nuclear translocation of p53, initiating the expression of multiple target genes. These transcriptional programs may be cell-type- and stimulus-specific, as is their outcome that ultimately imposes a barrier to cellular transformation. Cell cycle arrest and cell death are two well-studied consequences of p53 activation, but, while being considered critical, they do not fully explain the consequences of p53 loss-of-function phenotypes in cancer. Here, we discuss how mitotic errors alert the p53 network and give an overview of multiple ways that p53 can trigger cell death. We argue that a comparative analysis of different types of p53 responses, elicited by different triggers in a time-resolved manner in well-defined model systems, is critical to understand the cell-type-specific cell fate induced by p53 upon its activation in order to resolve the remaining mystery of its tumor-suppressive function.
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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.