ArticleOncogene2017
Mdm2 selectively suppresses DNA damage arising from inhibition of topoisomerase II independent of p53.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Quantitative Single-Cell Comparison of Sensitization to Radiation and a Radiomimetic Drug for Diverse Gold Nanoparticle Coatings.Small science · 2024Article
- Targeting drug resistance in glioblastoma (Review).International journal of oncology · 2024Review
- MDM2 provides TOP2 poison resistance by promoting proteolysis of TOP2βcc in a p53-independent manner.Cell death & disease · 2024Article
- Article
- Regulation of topoisomerase II stability and activity by ubiquitination and SUMOylation: clinical implications for cancer chemotherapy.Molecular biology reports · 2021Review
- The roles and regulation of MDM2 and MDMX: it is not just about p53.Genes & development · 2021Review
- The interplay between DNA topoisomerase 2α post-translational modifications and drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2020Review
- Degree ofThe oncologist · 2019Article
- Inhibition of DYRK1A-EGFR axis by p53-MDM2 cascade mediates the induction of cellular senescence.Cell death & disease · 2019Article
- The Role of MDM2 in Promoting Genome Stability versus Instability.International journal of molecular sciences · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mdm2 is often overexpressed in tumors that retain wild-type TP53 but may affect therapeutic response independently of p53. Herein is shown that tumor cells with MDM2 amplification are selectively resistant to treatment with topoisomerase II poisons but not other DNA damaging agents. Tumor cells that overexpress Mdm2 have reduced DNA double-strand breaks in response to doxorubicin or etoposide. This latter result is not due to altered drug uptake. The selective attenuation of DNA damage in response to these agents is dependent on both Mdm2 levels and an intact ubiquitin ligase function. These findings reveal a novel, p53-independent activity of Mdm2 and have important implications for the choice of chemotherapeutic agents in the treatment of Mdm2-overexpressing tumors.
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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.