Authors
Athanasios Niotis, Sofianiki Mastronikoli, Despoina Spyropoulou, Maria Adamopoulou, Panagiotis Fotiades, Antonios Vylliotis, Alexandros Tsantoulas, Evangelos Tsiambas
Published in
Maedica. Volume 21. Issue 2. Pages 490-494.
Abstract
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.
The aim of the current molecular review was to investigate the MDM2 oncogene deregulation mechanisms in BAC and the corresponding targeted therapeutic approaches.
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.
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.
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.
PMID:
42416752
Bibliographic data and abstract were imported from PubMed on 08 Jul 2026.
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