ReviewMaedica2026
Targeting Mouse Double Minute 2 Homolog (MDM2) Oncogene in Breast Adenocarcinoma.
Review in Maedica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Breast adenocarcinoma (BAC) is a leading cause of cancer-dependent morbidity and mortality in females worldwide. Concerning critical genes that are implicated in its onset and progression in BAC, the tumor suppressor protein Tp53 (gene locus: 17p13.1) and its negative regulator the Mouse Double Minute 2 Homolog (MDM2) - an oncogene (gene locus: 12q14.3) - form a significant feedback loop. Objective: The aim of the current molecular review was to investigate the MDM2 oncogene deregulation mechanisms in BAC and the corresponding targeted therapeutic approaches. Material and method: A set of fifty (n=50) published papers in the international database of PubMed was selected based on the new exposed knowledge in the field of mdm2 gene and protein normal function and deregulation. They also focused on the anti-mdm2 targeted regimens in BAC. The following keywords were used: breast, cancer, oncogene, mdm2, targeted therapies. Results: Mdm2 oncogene amplification - combined or not with specific gene polymorphisms - is a crucial molecular event in BAC onset and progression. These genetic alterations negatively affect the Tp53-MDM2 balance and cell homeostasis in breast epithelia. Conclusions: MDM2 oncogene overexpression - due predominantly to amplification - is a relatively frequent event in BAC. Understanding the impact of mdm2 on genetic substrate and biological behavior of BAC, many study groups have experimentally explored the role of specific anti-mdm2 agents and suggested a fragment of them for targeting its oncogenic activity in BACs characterized by specific genetic signatures.
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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 Socratic graph.