ReviewCancer science2010
The cell death machinery governed by the p53 tumor suppressor in response to DNA damage.
Review in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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
60 citing papers in PubMed, 112 citations in OpenAlex.
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- Insights into the Interaction Mechanisms of Peptide and Non-Peptide Inhibitors with MDM2 Using Gaussian-Accelerated Molecular Dynamics Simulations and Deep Learning.Molecules (Basel, Switzerland) · 2024Article
- Comprehensive Management of Stroke: From Mechanisms to Therapeutic Approaches.International journal of molecular sciences · 2024Review
- Natural products and the balancing act of autophagy-dependent/independent ferroptosis in cancer therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
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- New Insights into the Roles of p53 in Central Nervous System Diseases.The international journal of neuropsychopharmacology · 2023Review
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- Biophysics at the edge of life and death: radical control of apoptotic mechanisms.Frontiers in cell death · 2023Article
- KMU-191 Induces Apoptosis in Human Clear Cell Renal Cell Carcinoma Caki Cells Through Modulation of Bcl-xL, Mcl-1 (L), c-FLIP (L), and p53 Proteins.Journal of Cancer · 2023Article
- IND-2, a Quinoline Derivative, Inhibits the Proliferation of Prostate Cancer Cells by Inducing Oxidative Stress, Apoptosis and Inhibiting Topoisomerase II.Life (Basel, Switzerland) · 2022Article
- A Comprehensive Analysis and Anti-Cancer Activities of Quercetin in ROS-Mediated Cancer and Cancer Stem Cells.International journal of molecular sciences · 2022Review
- Thymol has anticancer effects in U-87 human malignant glioblastoma cells.Molecular biology reports · 2022Article
- CircSCAP interacts with SF3A3 to inhibit the malignance of non-small cell lung cancer by activating p53 signaling.Journal of experimental & clinical cancer research : CR · 2022Article
- Effects of Polyphenols on Oxidative Stress, Inflammation, and Interconnected Pathways during Spinal Cord Injury.Oxidative medicine and cellular longevity · 2022Review
- Crosstalk Between the Oxidative Stress and Glia Cells After Stroke: From Mechanism to Therapies.Frontiers in immunology · 2022Review
- Signature based on RNA-binding protein-related genes for predicting prognosis and guiding therapy in non-small cell lung cancer.Frontiers in genetics · 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cellular response to genotoxic stress that damages DNA includes cell cycle arrest, activation of DNA repair, and in the event of irreparable damage, induction of apoptosis. However, the signals that determine cell fate, that is, survival or apoptosis, are largely unclear. The tumor suppressor p53 has been implicated in many important cellular processes, including regulation of apoptotic cell death. When cells encounter genotoxic stress, certain sensors for DNA lesions eventually stabilize and activate p53. Subsequently, p53 exerts its tumor suppressor function by transactivating numerous target genes. Active p53 is subjected to a complex and diverse array of covalent post-translational modifications, which selectively influence the expression of p53 target genes. In this regard, the molecular basis for how p53 induces apoptosis has been extensively studied; however, the relative contribution of each downstream effector is still to be explored. Moreover, little is known about precise mechanisms by which modified p53 is capable of apoptosis induction. A thorough understanding for the whole picture of p53 modification in apoptosis will be extremely valuable in the development of highly effective and specific therapies for cancer patients. This review is focused on the current views regarding the regulation of cell fate by p53 in the apoptotic response to DNA damage.
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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.