ArticleGenes & cancer2012
Protecting the genome from mdm2 and mdmx.
Article in Genes & cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 20 citations in OpenAlex.
- MDM2-amplified esophageal adenocarcinomas exhibit an activated metabolic and immunosuppressive phenotype with multiple potential therapeutic targets.BMC cancer · 2025Article
- Targeting p53-MDM2 interaction by small-molecule inhibitors: learning from MDM2 inhibitors in clinical trials.Journal of hematology & oncology · 2022Review
- Review
- MDM2 and MDMX promote ferroptosis by PPARα-mediated lipid remodeling.Genes & development · 2020Article
- Role of Mdm2 and Mdmx in DNA repair.Journal of molecular cell biology · 2017Review
- Anatomy of Mdm2 and Mdm4 in evolution.Journal of molecular cell biology · 2017Review
- Genome Stability Requires p53.Cold Spring Harbor perspectives in medicine · 2016Review
- The Roles of MDM2 and MDMX in Cancer.Annual review of pathology · 2016Review
- Pharmacologically Increasing Mdm2 Inhibits DNA Repair and Cooperates with Genotoxic Agents to Kill p53-Inactivated Ovarian Cancer Cells.Molecular cancer research : MCR · 2015Article
- Article
- The Mdm network and its regulation of p53 activities: a rheostat of cancer risk.Human mutation · 2014Review
- RABL6A, a novel RAB-like protein, controls centrosome amplification and chromosome instability in primary fibroblasts.PloS one · 2013Article
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
Abstract
The contribution of Mdm2, and its recently identified family member Mdmx (Mdm4), to tumorigenesis has primarily focused on their negative regulation of the p53 tumor suppressor. Although Mdm2 and Mdmx clearly inhibit p53, which can lead to tumor development, both have also been shown to affect tumorigenesis independent of p53. Given that Mdm2 and/or Mdmx overexpression is common and likely underestimated in human cancers, understanding the functions of these proteins beyond p53 control is critical. In recent years, new functions of Mdm2 and Mdmx that lead to genome instability, a hallmark of malignancy, have emerged. Specifically, roles in the DNA damage response that are distinct from their regulation of p53 have been identified. Inhibition of p53 as well as other components of the DNA damage response by Mdm2 and Mdmx can result in delayed DNA repair and increased genome instability, making Mdm2 and Mdmx a danger to the genome when aberrantly expressed. However, the genome instability caused by altered levels of Mdm2 and Mdmx could be used therapeutically for the treatment of cancer. Specifically, drugs/small molecules that target the interaction between Mdm2 and p53 can stabilize Mdm2, resulting in negative consequences on the genome that could be exploited for cancer treatment, particularly malignancies lacking functional p53.
Indexed as
Identifiers
What 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.