ReviewCold Spring Harbor perspectives in biology2010
p53-based cancer therapy.
Review in Cold Spring Harbor perspectives in biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
125 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Recombinant Human Adenovirus-p53 Therapy for the Treatment of Cervical Cancer: A Meta-Analysis.Frontiers in oncology · 2021Pooled it
- Nucleic Acid Therapeutics for "Undruggable" Cancer Targets: Mechanisms, Challenges, and Prospects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Mutant p53-specific CD8TCR-therapy combined with a CD4TCR prevents relapse of cancer and outgrowth of micrometastases.Oncoimmunology · 2025Article
- Multi-Step Synthesis of Chimeric Nutlin-DCA Compounds Targeting Dual Pathways for Treatment of Cancer.Molecules (Basel, Switzerland) · 2025Article
- An engineered glutamic acid tRNA for efficient suppression of pathogenic nonsense mutations.Nucleic acids research · 2025Article
- Current Development of Therapeutic Vaccines in Lung Cancer.Vaccines · 2025Review
- Side-stepping the guardian of the genome: current cancer therapeutics targeting mutant p53.Frontiers in pharmacology · 2025Review
- p53 stabilisation potentiates [European journal of nuclear medicine and molecular imaging · 2024Article
- Inhibition of PRL2 Upregulates PTEN and Attenuates Tumor Growth in Tp53-deficient Sarcoma and Lymphoma Mouse Models.Cancer research communications · 2024Article
- Genetic heterogeneity in p53-null leukemia increases transiently with spindle assembly checkpoint inhibition and is not rescued by p53.Chromosoma · 2024Article
- C-C motif chemokine CCL11 is a novel regulator and a potential therapeutic target in non-alcoholic fatty liver disease.JHEP reports : innovation in hepatology · 2023Article
- Review
- Optimized spirooxindole-pyrazole hybrids targeting the p53-MDM2 interplay induce apoptosis and synergize with doxorubicin in A549 cells.Scientific reports · 2023Article
- Targeting USP2 regulation of VPRBP-mediated degradation of p53 and PD-L1 for cancer therapy.Nature communications · 2023Article
- Dual roles of TRIM3 in colorectal cancer by retaining p53 in the cytoplasm to decrease its nuclear expression.Cell death discovery · 2023Article
- A gene signature driven by abnormally methylated DEGs was developed for TP53 wild-type ovarian cancer samples by integrative omics analysis of DNA methylation and gene expression data.Annals of translational medicine · 2023Article
- Identification of a novel glycolysis-related prognosis risk signature in triple-negative breast cancer.Frontiers in oncology · 2023Article
- Insights into Regulators of p53 Acetylation.Cells · 2022Review
- GOF Mutant p53 in Cancers: A Therapeutic Challenge.Cancers · 2022Review
- p53 amyloid aggregation in cancer: function, mechanism, and therapy.Experimental hematology & oncology · 2022Review
65 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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inactivation of p53 functions is an almost universal feature of human cancer cells. This has spurred a tremendous effort to develop p53 based cancer therapies. Gene therapy using wild-type p53, delivered by adenovirus vectors, is now in widespread use in China. Other biologic approaches include the development of oncolytic viruses designed to replicate and kill only p53 defective cells and also the development of siRNA and antisense RNA's that activate p53 by inhibiting the function of the negative regulators Mdm2, MdmX, and HPV E6. The altered processing of p53 that occurs in tumor cells can elicit T-cell and B-cell responses to p53 that could be effective in eliminating cancer cells and p53 based vaccines are now in clinical trial. A number of small molecules that directly or indirectly activate the p53 response have also reached the clinic, of which the most advanced are the p53 mdm2 interaction inhibitors. Increased understanding of the p53 response is also allowing the development of powerful drug combinations that may increase the selectivity and safety of chemotherapy, by selective protection of normal cells and tissues.
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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.