ReviewMolekuliarnaia biologiia
[The use of p53 as a tool for human cancer therapy].
Review in Molekuliarnaia biologiia. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 20 citations in OpenAlex.
- Differential miRNA Expression in Human Macrophage-Like Cells Infected withJournal of fungi (Basel, Switzerland) · 2021Article
- Molecular subtyping of colorectal cancer: Recent progress, new challenges and emerging opportunities.Seminars in cancer biology · 2019Review
- Anti-cancer Potential of Captopril and Botulinum Toxin Type-A and Associated p53 Gene Apototic Stimulating Activity.Iranian journal of pharmaceutical research : IJPR · 2019Article
- Important molecular genetic markers of colorectal cancer.Oncotarget · 2016Review
- Assessing cell and organ senescence biomarkers.Circulation research · 2012Review
- Noninvasive assessment of regulable transferred-p53 gene expression and evaluation of therapeutic response with FDG-PET in tumor model.Gene therapy · 2010Article
- Versatile functions of p53 protein in multicellular organisms.Biochemistry. Biokhimiia · 2007Review
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
Abstract
The p53 tumor suppressor is a central component of a system that reinforces genetic stability of somatic cells in animals and humans. Inactivation of this gene occurs virtually in every cancer case, which eliminates results in further rapid accumulation of additional mutations leading to progression of a cancer cell toward more malignant phenotype. The mechanisms of p53 inhibition in cancer include point mutations leading to accumulation of inactive protein, deletion of the whole gene, or its portion, alteration in the genes involved in regulation of activity of p53, and defects in the genes controlled by p53. In addition, oncogenic viruses encode specialized proteins that are entitled to modify p53 functions in order to provide optimal condition for replication of viral genome. These viral proteins play central role in viral carcinogenesis, including 95% of cases of cervical carcinoma in women. The approacheas to restoration of p53 activity depend on particular type of alteration within the p53 pathway. In some cases an effective mean would be introduction of exogenous p53, particularly with the use of adenoviral vectors. There are also approaches in development that target reactivation of mutant proteins, or suppress natural inhibitors of p53. The review summarizes various schemes for therapy and prevention of cancer that are based on our knowledge of the p53 gene functions. Potential usefulness of the approaches for practical applications is discussed.
Indexed as
Identifiers
18318112PMC2634859W2616116563What 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.