ReviewThe Biochemical journal2000
Strategies for manipulating the p53 pathway in the treatment of human cancer.
Review in The Biochemical journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 146 citations in OpenAlex.
- ATM and p53 in aging and cancer: a double-edged sword in genomic integrity.Biogerontology · 2025Review
- Epidermal growth factor receptor activity is elevated in glioma cancer stem cells and is required to maintain chemotherapy and radiation resistance.Oncotarget · 2017Article
- Article
- Loss of LZAP inactivates p53 and regulates sensitivity of cells to DNA damage in a p53-dependent manner.Oncogenesis · 2017Article
- An Algorithm for Finding the Singleton Attractors and Pre-Images in Strong-Inhibition Boolean Networks.PloS one · 2016Article
- Discovery of PI-1840, a novel noncovalent and rapidly reversible proteasome inhibitor with anti-tumor activity.The Journal of biological chemistry · 2014Article
- Feline mammary carcinoma stem cells are tumorigenic, radioresistant, chemoresistant and defective in activation of the ATM/p53 DNA damage pathway.Veterinary journal (London, England : 1997) · 2013Article
- Bcl-3 regulates UVB-induced apoptosis.Human cell · 2013Article
- TIP30 directly binds p53 tumor suppressor protein in vitro.Molecules and cells · 2012Article
- Ubiquitin proteasomal pathway mediated degradation of p53 in melanoma.Archives of biochemistry and biophysics · 2011Article
- Defining the molecular nexus of cancer, type 2 diabetes and cardiovascular disease.Current molecular medicine · 2010Review
- HDMX-L is expressed from a functional p53-responsive promoter in the first intron of the HDMX gene and participates in an autoregulatory feedback loop to control p53 activity.The Journal of biological chemistry · 2010Article
- Dual-specificity phosphatase 26 is a novel p53 phosphatase and inhibits p53 tumor suppressor functions in human neuroblastoma.Oncogene · 2010Article
- Targeting p53 for Novel Anticancer Therapy.Translational oncology · 2010Article
- Article
- Recent advances in validating MDM2 as a cancer target.Anti-cancer agents in medicinal chemistry · 2009Review
- Structural and functional implications of p53 missense cancer mutations.PMC biophysics · 2009Article
- Knitting and untying the protein network: modulation of protein ensembles as a therapeutic strategy.Protein science : a publication of the Protein Society · 2009Review
- MDM2 SNP309 is associated with high grade node positive breast tumours and is in linkage disequilibrium with a novel MDM2 intron 1 polymorphism.BMC cancer · 2008Article
- Novel role of p53 in maintaining mitochondrial genetic stability through interaction with DNA Pol gamma.The EMBO journal · 2005Article
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
Human cancer progression is driven in part by the mutation of oncogenes and tumour-suppressor genes which, under selective environmental pressures, give rise to evolving populations of biochemically altered cells with enhanced tumorigenic and metastatic potential. Given that human cancers are biologically and pathologically quite distinct, it has been quite surprising that a common event, perturbation of the p53 pathway, occurs in most if not all types of human cancers. The central role of p53 as a tumour-suppressor protein has fuelled interest in defining its mechanism of function and regulation, determining how its inactivation facilitates cancer progression, and exploring the possibility of restoring p53 function for therapeutic benefit. This review will highlight the key biochemical properties of p53 protein that affect its tumour-suppressor function and the experimental strategies that have been developed for the re-activation of the p53 pathway in cancers.
Indexed as
Identifiers
11062053PMC1221427W2171732847What 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.