ArticleIranian journal of medical sciences2012
The role of tumor protein 53 mutations in common human cancers and targeting the murine double minute 2-p53 interaction for cancer therapy.
Article in Iranian journal of medical sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Opportunities in cancer gene therapy: inhibiting MDM2 and restoring p14ARF as a means to activate p53.Molecular and cellular biochemistry · 2026Review
- Emerging therapeutic advancements in pancreatic cancer: a contemporary review.Discover oncology · 2025Review
- TP53 mutation status and consensus molecular subtypes of colorectal cancer in patients from Rwanda.BMC cancer · 2024Article
- Hereditary Gastrointestinal Tumor Syndromes: When Risk Comes with Your Genes.Current issues in molecular biology · 2024Review
- Revolutionizing pediatric neuroblastoma treatment: unraveling new molecular targets for precision interventions.Frontiers in cell and developmental biology · 2024Review
- Efficacy of metformin and electrical pulses in breast cancer MDA-MB-231 cells.Exploration of targeted anti-tumor therapy · 2024Article
- Encephalomalacia/gliosis, deep venous thrombosis, and cancer in Arg393His antithrombin Hanoi and the potential impact of the β-amyloid precursor protein (APP) on thrombosis and cancer.AIMS neuroscience · 2022Review
- Biomolecular Factors Represented by Bcl-2, p53, and Tumor-Infiltrating Lymphocytes Predict Response for Adjuvant Anthracycline Chemotherapy in Patients with Early Triple-Negative Breast Cancer.Cancer management and research · 2020Review
- Wee1 kinase inhibitor MK-1775 induces apoptosis of acute lymphoblastic leukemia cells and enhances the efficacy of doxorubicin involving downregulation of Notch pathway.Oncology letters · 2018Article
- Overexpression of p53 delivered using recombinant NDV induces apoptosis in glioma cells by regulating the apoptotic signaling pathway.Experimental and therapeutic medicine · 2018Article
- Dissect the Dynamic Molecular Circuits of Cell Cycle Control through Network Evolution Model.BioMed research international · 2017Article
- The Increased Level of Serum p53 in Hepatitis B-Associated Liver Cirrhosis.Iranian journal of medical sciences · 2014Article
- miR-19b promotes tumor growth and metastasis via targeting TP53.RNA (New York, N.Y.) · 2014Article
- Does not hUTP14a promoter form a regulation feedback loop with P53?Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2014Article
- Detection of TP53 R249 Mutation in Iranian Patients with Pancreatic Cancer.Journal of oncology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The gene TP53 (also known as protein 53 or tumor protein 53), encoding transcription factor P53, is mutated or deleted in half of human cancers, demonstrating the crucial role of P53 in tumor suppression. There are reports of nearly 250 independent germ line TP53 mutations in over 100 publications. The P53 protein has the structure of a transcription factor and, is made up of several domains. The main function of P53 is to organize cell defense against cancerous transformation. P53 is a potent transcription factor that is activated in response to diverse stresses, leading to the induction of cell cycle arrest, apoptosis or senescence. The P53 tumor suppressor is negatively regulated in cells by the murine double minute 2 (MDM2) protein. Murine double minute 2 favors its nuclear export, and stimulates its degradation. Inhibitors of the P53-MDM2 interaction might be attractive new anticancer agents that could be used to activate wild-type P53 in tumors. Down regulation of MDM2 using an small interfering RNA (siRNA) approach has recently provided evidence for a new role of MDM2 in the P53 response, by modulating the inhibition of the cyclindependent kinase 2 (cdk2) by P21/WAF1 (also known as cyclin-dependent kinase inhibitor 1 or CDK-interacting protein 1).
Indexed as
Identifiers
23115424PMC3470295W2157238757What OpenQuestion 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 OpenQuestion graph.